Given the role of myeloid AMPK signaling in modulating macrophage polarization in the context of adipose tissue inflammation (23), skeletal muscle regeneration (28, 29) and atherosclerosis (30, 31, 32, 33), we sought to clarify if AMPK signaling in resident and infiltrating liver macrophages was protective in a CDAHFD-induced NASH model. This evidence concerns the gene PRKAA2 and metabolic dysfunction-associated steatohepatitis.