We therefore tested whether targeting only neutrophil accumulation independently of macrophages—whose role is already well-established in the progression of NAFLD/NASH [24–35]—could improve insulin sensitivity, prevent the progression of HFD-induced IR, and possibly prevent the progression towards a liver pathology that could be prodromal of, and/or precipitate NAFLD/NASH. Here, INS is linked to metabolic dysfunction-associated steatohepatitis.