demonstrated the plasticity of ILC1s showing a conversion of NK (defined as Lin-negative NK1.1+CD49a−CD49b+) cells into ILC1-like cells (CD200r1+ CD49a+) in mice with non-alcoholic fatty liver disease (31), thus indicating that cNKs could also differentiate into proinflammatory ILC1s in our HFD IRI model thereby exacerbating hepatocellular injury via IFN-γ upon IRI in the setting of hepatic steatosis, where the same degree of injury may not be appreciated in non-steatotic livers. This evidence concerns the gene IFNG and fatty liver disease.