Our previous study demonstrated that disruption of the AMPK-TBC1D1 axis increases lipogenesis in the adipose tissue and causes obesity and type 2 diabetes by promoting IGF1 vesicle secretion in a TBC1D1S231A-knock-in (KI) mouse model from 2 to 10 months [9]. Here, IGF1 is linked to obesity due to melanocortin 4 receptor deficiency.