PRKAA1 and Autoimmunity: For example, the ULK1 complex, which promotes autophagy, is inhibited and activated by mTORC1 and AMPK signaling, respectively.172,173,234,235 Further, autophagy may act as an ‘off-switch’ for mTORC1 activation and glycolysis under nutrient-deficient conditions.26 This inhibition likely favors cell survival and maintains cellular quiescence at the expense of cell growth and proliferation.243 Understanding the mechanisms for the interplay between autophagy and mTORC1 may be therapeutically relevant for immune-related diseases, such as autoimmune disorders and cancer.