TLR4 and p65 expression levels in macrophages were significantly reduced after treatment with let7b, whereas p-STAT3 and p-AKT expression levels were significantly time-dependently upregulated, promoting macrophage differentiation to M2 type, and STAT3 activation was completely inhibited in the presence of let-7b inhibitor, suggesting that regulation of macrophage polarization can be mediated through TLR4/NF-κB/STAT3/AKT regulatory signaling, which in turn produces a large number of mediators that fine-tune the inflammatory response and promote wound healing in diabetic skin wounds (80). This evidence concerns the gene STAT3 and diabetes mellitus.