Infiltration of conventional T lymphocytes into the liver parenchyma is increasingly recognized as a hallmark of MASH, and the modulation of T-cell recruitment or function has been shown to impact MASH severity in preclinical models.6–8 However, a deep understanding of CD4+ T-cell phenotype and function in MASH has been limited, despite their potential to orchestrate immune responses in inflamed tissues. This evidence concerns the gene CD4 and metabolic dysfunction-associated steatohepatitis.