We selected a PTEN liver-KO steatotic mouse model instead of Western diet feeding models for key advantages: (1) PTEN loss either through genetic mutations or epigenetic silencing is a well-established etiological factor in human liver disease that reliably induces steatosis without dietary variability [23]; (2) PTEN inhibits AKT activity whereas loss of PTEN unleashes the inhibition and AKT overactivation leads to excessive lipogenesis and steatosis [24]. The gene discussed is AKT1; the disease is steatosis.