GARS1 and neuropathy: Finally, transgenic overexpression of wild-type GARS completely rescues the embryonic lethality of both point mutations in combination with the null allele, but does nothing to correct the neuropathy, suggesting that there are loss of function aspects of the point mutations that impair viability, but that the neuropathy is the result of a pathological gain-of-function that the wild-type protein cannot out compete (Motley et al., 2011).