PLA2G4A and atherosclerosis: Fat-1 directly increases the content of endogenous PUFAs, mainly n-3 PUFAs, as a signal transduction molecule by facilitating the nuclear localization of PPARα to activate the PPARα-mediated signaling pathway, thereby enhancing FAO, inhibiting DNL synthesis, and suppressing inflammation mediated by p38 MAPK/cPLA2 and then ultimately alleviating MAFLD and atherosclerosis development (Fig. 9).