Cytokines are major mediators of this inflammatory state: some of them seem to be predominantly protective (TWEAK, IL-10, IL-22, IL-25, IL-27), others appear to exhibit a dual-faceted effect, depending on the stage of MASLD (TNF-α, TRAIL, IL-2, IL-6, IL-18, IL-33, IFNs), whereas a third group of cytokines seems to be predominantly harmful, thus driving the progression of hepatic steatosis to MASH, fibrosis, cirrhosis, and possibly to HCC. The gene discussed is TNF; the disease is fibrosis.