H2AB1 and Insulin resistance: Stables et al. (2011) also reported that compared to macrophages from hyper-inflamed mice with naïve and pro-inflammatory macrophages from the un-inflamed peritoneum, H2-Ab1 and Cd74 were enriched for antigen processing/presentation. Deng et al. (2017) found that the genetic defect of H2-Ab1 in adipocytes can reduce IFNγ and increase Treg content in mice fat, which leads to a decrease in fat inflammation and insulin resistance caused by obesity. In a word, the hub genes screened out in DEGs also contribute to the key pathways such as immune response and inflammatory response (Figure 4C).