Given the crucial of FAK activation in NASH progression and to further confirm the potential suppressive effects of DUSP22 on FAK signaling in vivo, hepatocyte-specific FAK knockout (FAKHepKO) (Supplementary Fig. 21a–c), and hepatocyte-specific DUSP22 and FAK double deletion (Hep-DKO) mice were thereafter generated (Supplementary Fig. 21d). The gene discussed is PTK2; the disease is metabolic dysfunction-associated steatohepatitis.