The deactivation of AMPK by TNF-α in skeletal muscle and adipose tissue in mice with obesity and diabetes involves the de novo synthesis of protein phosphatase 2C PP2C, a ubiquitous Ser/Thr protein phosphatase [83,84,85] that dephosphorylates p-AMPK-α (Thr172), effectively deactivating AMPK. The gene discussed is PRKAA1; the disease is obesity due to melanocortin 4 receptor deficiency.