In obesity, both liver resident (e.g., Kupffer cells, [KC], hepatic stellate cells, [HSC], hepatocytes) and infiltrating immune cells (e.g., neutrophils, dendritic cells [DC], natural killer [NK] cells, NKT cells, blood monocytes, T cells, B cells, and macrophages) contribute to NAFLD development and progression via systemic and tissue inflammatory mediator production (e.g., interleukin [IL]-17A, IL-6, tumor necrosis factor [TNF], IL-1β) (5, 11). This evidence concerns the gene CALCA and metabolic dysfunction-associated steatotic liver disease.