While the role of innate immunity, particularly pro-inflammatory macrophages, has been extensively demonstrated in mice and humans,4,5 increasing evidence points to the role of adaptive immunity in the pathophysiology of MASH.[6], [7], [8] CD4+ T cells likely play an important role in the development and progression of MASH, as increased numbers of intrahepatic TH17 cells have been reported in mice and patients with MASH.6 The gene discussed is CD4; the disease is metabolic dysfunction-associated steatohepatitis.