There are several pathways for Kupffer cell activation in NAFLD: via gut-derived endotoxins, such as LPS entering the circulation owing to enhanced intestinal permeability and acting through Toll-like receptors (TLRs); via molecules associated with hepatocyte damage, such as histidine-rich glycoprotein and danger-associated molecular patterns; via free fatty acids through TLRs and adipokines (leptin via the leptin receptor (LEPR) in the adipose tissue); and via cholesterol and its metabolites acting through CD36 and scavenger receptor A (SRA) [20]. Here, CD36 is linked to metabolic dysfunction-associated steatotic liver disease.