The complete and faster regression of steatosis after administration of Ang-(3–4) also entails accentuated, rapid, and continuous lipolysis, probably resulting from the activation of both the adipose triglyceride lipase (ATGL) by cyclic AMP-dependent protein kinase (PKA) [20] and the hormone-sensitive lipase (HSL) by catecholamines [21], whose defects play a central role in obesity [22]. Here, PNPLA2 is linked to obesity due to melanocortin 4 receptor deficiency.