The observed pattern mirrors the biphasic immunopathology seen in sepsis, where MASLD patients exhibited higher baseline levels of IL17A, IL-23, IL-33, CXCL10 and TGF-β1, yet experienced steeper declines in in IL-10, IL-23, CXCL10 and TGF-β1 in comparison to non-MASLD counterparts [32]. The gene discussed is IL33; the disease is metabolic dysfunction-associated steatotic liver disease.