NFKB1 and type 2 diabetes mellitus: Upon binding with IL-1β, the receptor activates the NF-κB pathway, further promoting the production of IL-1β, thereby expanding the scope of inflammation, causing dysfunction and damage to islet β-cells, and ultimately leading to reduced insulin secretion.[19] p-Hydroxybenzaldehyde-D5, a deuterated derivative, shows theoretical antioxidative benefits for T2DM-related oxidative stress, but empirical evidence remains lacking.