We have reported that: (1) STK25 mRNA and protein levels positively correlate with the severity of MASH in human liver biopsies12, 13, 14; (2) STK25 knockdown in cultured human hepatocytes reduces ectopic fat accumulation by causing a shift from lipid anabolism towards catabolism12,13,15; and (3) genetic and pharmacologic inactivation of STK25 in mice ameliorates the full spectrum of diet-induced MASH, including protection against liver steatosis, inflammation, and fibrosis.12 This evidence concerns the gene STK25 and fatty liver disease.