As a substantial portion of Huntington's disease neurotoxicity results from a deficiency in the transsulfuration pathway through the interaction of Huntingtin with cystathionine β-synthase64 and the inhibition of cystathionine-γ lyase transcription activator by mutant Huntingtin61, the activation of SpCAT observed in our cellular model of Huntington's disease, probably due to the post-translational modification of CAT promoted by non-receptor protein tyrosine kinases65, may participate in compensatory mechanisms activated by imbalances in the equilibrium of biological thiols. The gene discussed is CAT; the disease is Huntington disease.