Thus, our findings suggest that REDD1-mediated atypical NF-κB activation and proinflammatory cytokine production in lipid-laden adipocytes and adipose tissue macrophages are causative factors for inducing global insulin resistance, consistent with results reported in NF-κB p50−/− mice25, further underscoring the crucial role of REDD1 in the pathogenesis of meta-inflammation, insulin resistance, and T2D through atypical NF-κB activation. This evidence concerns the gene DDIT4 and type 2 diabetes mellitus.