AKT1 and Prader-Willi syndrome: There is subsequent activation of various kinases during different stages of PWS [7]: (1) JNKs and ERKs are firstly and consecutively activated in all PWS tissues, which may contribute to both the pathogenesis and progressive development of PWS; (2) AKT and PI3K are subsequently activated and may be involved in hypertrophic PWS blood vessels; and (3) phosphoinositide phospholipase C γ subunit (PLC-γ), PI3K and protein kinase C (PKC) are activated in the most advanced stage of PWS and participate in nodule formation [7,8].