In support of these data in murine NASH, human liver CD8+ T cells characterised by high levels of CD69 expression have also been reported to promote bystander, non-antigen specific liver damage via IL-15-induced pathways; sinusoidal CD69+CD8+ TRM with increased HIF2α and NKG2D expression positively correlated with the degree of liver failure and disease severity in patients with ongoing liver damage resulting in end-stage cirrhosis [29]. The gene discussed is CD8A; the disease is metabolic dysfunction-associated steatohepatitis.