In this study, overexpression of PTEN prevented AKT signaling activation in Q74 cells, thereby reversing the inhibition of apoptosis and ROS by USP11 knockdown, which was consistent with previous findings and suggested that the USP11/PTEN/AKT axis was involved in the regulation of oxidative stress and neuronal damage during HD progression. This evidence concerns the gene AKT1 and Huntington disease.