FBXL6 and metabolic dysfunction-associated steatotic liver disease: An increase in ACh levels to activate AChRs on hepatocytes or resident hepatic cells, including Kupffer cells and satellite cells, has been reported to alleviate NAFLD and alcohol‐associated liver injury.[62, 63, 64] In contrast, in this study, irregular exercise increased ACh levels and was accompanied by FBXL6‐mediated neutrophil infiltration such that FBXL6 interacted with α7‐nAChRs to switch downstream signaling from anti‐inflammatory to proinflammatory signaling, altering the effect of ACh on NAFLD.