However, the vast majority of POMCCreGFP + cells continue expressing POMC throughout the adulthood [8] and the obesity phenotypes associated with POMCCre-restricted PI3K-Akt-mTOR pathway over-activation are largely explained by inactivation of POMC neurons [[10], [11], [12]]. This evidence concerns the gene AKT1 and obesity due to melanocortin 4 receptor deficiency.