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. This evidence concerns the gene IL33 and fibrosis.