The above considering, we could hypothesize that IL-17 may increase in early stages of MASLD to reverse hepatic steatosis; however, when this mechanism fails and the presence of IL-17 is elongated, then IL-17 may adversely affect hepatic inflammation and fibrosis, as supported for other adipokines and cytokines [38]. The gene discussed is IL17A; the disease is metabolic dysfunction-associated steatotic liver disease.