Further, GSK3β and ERK likely have opposing roles during HD pathogenesis, with GSK3β inhibition rescuing pathogenic HTT-mediated axonal transport defects, synaptic dysfunction, and neuronal cell death (Fig. 4), and ERK inhibition enhancing these phenotypes (Fig. 6) and excess ERK rescuing HTT-containing accumulations caused by pathogenic HTT (Fig. 7). Here, GSK3B is linked to Huntington disease.