To further test whether the palmitoylation-depalmitoylation cycles of SMAD2 and STAT3 promoted Th17 cell differentiation and aggravated inflammation in vivo, we studied the effects of loss of DHHC7 and APT2 in a myelin oligodendrocyte glycoprotein (MOG35-55)–induced experimental autoimmune encephalomyelitis (EAE) mouse model, which is a classical experimental model for MS (39). The gene discussed is OMG; the disease is experimental autoimmune encephalomyelitis.