In conclusion our data demonstrate the implication of ICOS/ICOSL dyad in modulating the evolution of MASH and suggest that the interaction between ICOS+/CD8+ T lymphocytes and TREM2+ MoMFs through reverse ICOSL signalling might represent a novel mechanism by which adaptive immunity contributes to sustain hepatic inflammation and fibrosis in MASH. The gene discussed is ICOS; the disease is inflammatory response.