They not only inhibit the anti-inflammatory effects of regulatory T cells but also promote the pro-inflammatory effects of M1 macrophages [50].In contrast, low expression of NR4A1, IL6, and DHODH involves key pathways such as “glycosphingolipid biosynthesis,” “circadian rhythms” and “type 2 diabetes,” activating pro-inflammatory M1 macrophages. Here, NR4A1 is linked to type 2 diabetes mellitus.