IL-33 is also markedly upregulated in the T2D stage, which can competitively inhibit angiotensin II and phenylephrine, and over-activate the NF-κB and MAPK signaling pathways [68]; thus, the IL-33 and IL1RL1 complex can sustainably induce local inflammation in islet tissue during ND-T2D progression. Here, NFKB1 is linked to type 2 diabetes mellitus.