Similarly, a distinct population of inflammatory hepatic CXCR3+ Th17 cells emerges in MASLD, which are sufficient to increase chromatin accessibility, glycolytic skewing and concomitant production of IL-17A, IFNγ, and TNFα, thus exacerbating MASLD pathogenesis [74]. The gene discussed is CXCR3; the disease is metabolic dysfunction-associated steatotic liver disease.