In a mouse model of liver fibrosis that recapitulates the stepwise, clinically observed progression from nonalcoholic fatty liver disease (NAFLD, an increasingly common, known risk factor for liver-related mortality [92]) to nonalcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), pacritinib, presumably through IRAK1 signaling inhibition, significantly reduced liver fibrotic area compared with vehicle control without affecting steatosis [93]. The gene discussed is IRAK1; the disease is metabolic dysfunction-associated steatotic liver disease.