The research conducted by Su and colleagues revealed that miR-145-5p, transferred through extracellular vesicles (EVs), directly modulates the expression of the cyclin-dependent kinase inhibitor 1A (CDKN1A), consequently activating the Erk/Akt, thus promoting wound healing in high glucose (HG)-induced human dermal fibroblasts as well as in murine models of diabetes mellitus in vivo (70). This evidence concerns the gene CDKN1A and diabetes mellitus.