We organized findings across shared T2DM-relevant pathogenic modules, including PI3K/Akt and AMPK signaling, inflammatory outputs (NF-κB/NLRP3), redox regulation (NRF2/ROS), angiogenic signaling (VEGF), and gut-liver-brain-immune network interactions, emphasizing studies in which pathway modulation is accompanied by metabolic or complication-relevant endpoints. The gene discussed is NFKB1; the disease is type 2 diabetes mellitus.