We and other research groups also found that the inactivation of STK25 or MST3 in mice, either by genetic knockout or treatment with antisense oligonucleotides, improves whole-body insulin sensitivity and effectively ameliorates the full spectrum of diet-induced MASLD encompassing suppressed hepatic steatosis, inflammation, and fibrosis [36,42,43,44]. This evidence concerns the gene STK25 and metabolic dysfunction-associated steatotic liver disease.