Based on the ability of TgD to substitute for a wild type Gars allele in rescuing viability in combination with XM256, we hypothesized that a loss of function would be corrected by the presence of the transgene, whereas increased toxicity from the higher dose of mutant protein would not be corrected, based on the inability of the transgene to improve the neuropathy phenotype in C201R/+ mice. The gene discussed is GARS1; the disease is neuropathy.