The pathological prolongation of the inflammatory phase is a key factor contributing to impaired wound healing in diabetes [47], primarily due to persistent M1 macrophage polarization, elevated pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), ROS overproduction, and sustained AGE-RAGE signaling under chronic hyperglycemic conditions [48,49]. This evidence concerns the gene IL1B and diabetes mellitus.