Hence, we cannot exclude the possibility that the decreased aggregate numbers in the cerebellum of HD; Igf-1r hemizygous mice compared to control littermates, may be resulting from differential acute nutrient/IGF1/insulin signalling in the mice that may be sufficient to create a short-term relative difference in autophagy sufficient to impact on huntingtin aggregate numbers, even if the “steady-state” activity of the mTOR pathway were unchanged in these mice. The gene discussed is IGF1; the disease is Huntington disease.