The increasing links of altered autophagy with relevant pathological conditions, such as metabolic disorders, cancer, or cardiovascular diseases3–5, along with the central role of Gαq/11 and Gq-coupled GPCR in the same contexts55,56, suggest that the function or malfunction of this Gαq/mTORC1/autophagy modulation cascade may contribute to these pathological situations and constitute a potential therapeutic target. Here, GNAQ is linked to metabolic disease.