PTEN是INS-PI3K-AKT通路的负调控因子，对新陈代谢和细胞生长起至关重要的调节作用。在癌症中，PTEN是最常见的突变抑癌基因之一。然而，PTEN的过度表达能够延长雄性和雌性小鼠的寿命。我们最近的研究表明，在小鼠肝脏和培养细胞中，PTEN对启动分子伴侣介导的自噬（CMA）起到必需和充分的作用。当PTEN过度表达时，通过CMA选择性降解蛋白质是抑制糖酵解和脂肪酸合成所必需的。因此，PTEN下游的CMA的激活可能通过对关键代谢酶的选择性降解来调节健康和代谢。

PTEN is a negative modulator of the INS-PI3K-AKT pathway and is an essential regulator of metabolism and cell growth. PTEN is one of the most commonly mutated tumor suppressors in cancer. However, PTEN overexpression extends the lifespan of both sexes of mice. We recently showed that PTEN is necessary and sufficient to activate chaperone-mediated autophagy (CMA) in the mouse liver and cultured cells. Selective protein degradation via CMA is required to suppress glycolysis and fatty acid synthesis when PTEN is overexpressed. Thus, activation of CMA downstream of PTEN might modulate health and metabolism through selective degradation of key metabolic enzymes.