With respect to proliferative effects, our study did not directly quantify epithelial proliferation; however, our previous study indicates that rTMD1 preserves cellular viability/proliferation while restraining pathogenic ERK/HIF‐1α activity, suggesting that accelerated closure in diabetes likely reflects both relief of inflammatory impediments and maintenance of reparative capacity rather than indiscriminate mitogenic stimulation [13]. Here, HIF1A is linked to diabetes mellitus.