Consistent with this observation, the expression of PRMT5/methylosome protein 50 (MEP50) complexes, or the genetic ablation of the JMJD6 (H4R3Me2 demethylase), rescued the toxic effects of mutant Htt in primary cortical neurons [119], indicating that PRMT5 loss may be responsible, at least in part, for HD pathogenesis. Here, HTT is linked to Huntington disease.