Although the accumulation of mutant protein can lead to mTOR-independent autophagy with the degradation of accumulated proteins differing from the degradation under conditions of starvation (Yamamoto et al., 2006), dietary restriction in a HD mouse model resulted in an increase in autophagy and a reduction in mHtt aggregate formation and the normalization of blood glucose regulation, thereby contributing to a slower disease progression and an extended lifespan (Duan et al., 2003; Ehrnhoefer et al., 2018). This evidence concerns the gene MTOR and Huntington disease.