In a nonalcoholic fatty liver disease model, TIM-3 is shown to control liver-resident iNKT cell homeostasis with direct TIM-3 signaling inducing apoptosis and indirect signaling from IL-15, produced by TIM-3 stimulated Kupffer cells, promoting iNKT cell proliferation (46). Here, HAVCR2 is linked to metabolic dysfunction-associated steatotic liver disease.