There are some other things in ?genetic-modifications.csv.

Gene candidates for germline genetic modification

Direct gene candidates

CD47 suppression

gobs of radiation resistance. prevent binding of thrombospondin to CD47 with a drug, inhibits NO production and somehow this prevents radiation damage and kills cancer cells. antisense CD47 RNA should do the trick permanently.

Myostatin inhibition

There are a number of options here, but with germline modification, a muscle-specific knockout of ACVR2B or myostatin are good choices. Also follistatin overexpression in muscle.

PEPCK-C overexpression

In muscle, this allows greatly improved metabolism and endurance (see 'mighty mice'). Synergistic effect with myostatin inhibition is untested, but intriguing.

P53 overexpression

As the "guardian of the genome", p53 is missing in many cancers, and has been investigated as a gene therapy option for cancer. Introducing a separate copy, or copies of the gene from the wild-type could reduce the incidence of knockout mutations that normally lead to cancer.

Alpha-galactosidase expression

Humans are unsuited to digesting some types of branching carbohydrates, which then pass through the intestines and feed annoying bacteria. Not a huge priority, but with the increased metabolic demands from the muscle-enhancing therapies, it can't hurt.

CCR5 knockout

Provides resistance to HIV and plague. Increases risk from West Nile virus, but who gives a fuck about that.

Also see HCP5 (rs2395029), and CCL3L1.

LRP5 gene (strong bones)

Those with the LRP5 gene have extra strong bones.

PCSK5 (lower coronary disease)

Those with the PCSK5 gene have 88 percent lower coronary disease.

FUT2 (norovirus / stomach flu resistance)

Those with double FUT2 are resistant to stomach flu.


Lactase persistence (lactose tolerance);C)

Also known as "C/T(-13910)", and located in the MCM6 gene but with influence on the lactase LCT gene, rs4988235 is one of two SNPs that is associated with the primary haplotype associated with hypolactasia, more commonly known as lactose intolerance in European Caucasian populations. [PMID 11788828], [PMID 15114531]

In these populations, the rs4988235(T) allele is both the more common allele and the one associated with lactase persistence; individuals who are rs4988235(C;C) are likely to be lactose intolerant. In populations of sub-Saharan Africans, though, the rs4988235(T) allele is so rare that it's unlikely to be predictive of lactase persistence, and other SNPs are predictive instead. [PMID 15106124, PMID 17159977]

Hyperosmia (increased odor sensitivity)

rs1953558 - sensitivity to sweaty odor (isovaleric acid)

Pain sensitivity


Malaria resistance

DARC - rs2814778

HBB - i3003137

G6PD - rs1050828


sweetness - TAS1R2

umami - TAS1R1

sourness - PKD2L1

spiciness - TRPV1

signal - GNAT3, TRPM5, PLCB2

bitterness - TAS2R4, TAS2R5, TAS2R16, TAS2R8, TAS2R38, TAS2R48

Sprinting vs. endurance

ACTN3 - rs1815739

Theoretical "heterozygote advantages" genes

The principle here is that diseases such as sickle cell or Tay-Sachs, among many others, persist in a population because having one 'good' and one 'bad' copy of the gene offers a significant advantage - in disease resistance, intelligence, etc.

While it would be nice to find a point mutation that would mimic the benefits of heterozygosity, the most straightforward option would be to give someone both variants of the gene, with ~50% expression of each.

Other notes

Tetracycline response elements, i.e. tet-on and tet-off, can be used for transgenes where constant expression is undesirable. While a number of options for such inducible expression exist, the tet system is the most studied. It is left as an exercise to the reader to determine which genes would be suitable candidates [I will add some when I get around to it].

Candidate genes for sports doping

This is lifted from this table.

Gene/product System/organ targets Gene product properties Physiologic response
ACE skeletal muscles peptidyl dipeptidase ACE-D is involved in fast twitch muscles.
ACTN3 skeletal muscles actin-binding proteins related to dystrophin Involved in fast-twitch muscles.
endorphins central and peripheral nervous system widely active peptides pain modulation
EPO hematopoietic system glycoprotein hormone Increases RBC mass and oxygen delivery.
HGH endocrine system 191-amino acid protein Increases muscle size, power, and recovery.
HIF hematologic and immune systems multisubunit protein Regulates transcription at hypoxia response elements.
IGF-1 endocrine/metabolic/skeletal muscle 70-amino acid protein Increases muscle size, power, and recovery by increasing regulator cells.
myostatin skeletal muscle 2-subunit protein Regulates skeletal muscle. Inhibition increases muscle size, power, and recovery.
PPAR-delta skeletal muscle and adipose tissue nuclear hormone receptor protein Promotes fat metabolism and increases number of slow twitch fibers.
VEGF vascular endothelium glyosylated disulfide-bonded homodimers Induces development of new blood vessels.

Abbreviations: ACE, angiotensin-converting enzyme; ACTN3, actinin binding protein 3; EPO, erythropoetin; HGH, human growth factor; HIF, hypoxia inducible factor; IGF-1, insulin-like growth factor; PPAR-delta, peroxisome proliferators-activated receptor (delta); VEGF, vascular endothelial growth factor.


dental caries vaccine


a genetically modified strain of Streptococcus mutans called BCS3-L1, is incapable of producing lactic acid, which dissolves tooth enamel, and aggressively replaces native flora. In laboratory tests, rats who were given BCS3-L1 were conferred with a lifetime of protection against S. mutans. Dr. Jeffrey D. Hillman suggests that treatment with BCS3-L1 in humans could also provide a lifetime of protection, or, at worst, require occasional re-applications. He figures the treatment would be available in dentists' offices and "will probably cost less than $100.

paper: Genetically modified Streptococcus mutans for the prevention of dental caries


Originally authored by yashgaroth on 2012-06-28. See for more context.