To develop an iPSC-based model of hepatic insulin resistance and resolve the controversy about the impact of inflammation, we modified differentiation of iPSC-Heps to achieve physiologically relevant insulin sensitivity and co-cultured the cells with pro-inflammatory (classically activated; M1) or undifferentiated/non-activated (M0) macrophages derived from the same iPSC line (iPSC-Macs). This evidence concerns the gene INS and Insulin resistance.