Mice with a liver-specific pten deletion and mice with a liver-specific deletion of CMA receptor lamp2a show remarkably similar phenotypes, including spontaneous development of fatty liver disease, reductions in peripheral adiposity, and a shift in liver energy production favoring glycolysis over oxidative phosphorylation (Stiles et al., 2004; Schneider et al., 2014). The gene discussed is PTEN; the disease is fatty liver disease.