To determine the wound-healing activity of CDK1-loaded sEVs in vivo, we used 12- to 16-week-old leptin receptor knockout mice, an established and well-defined model of impaired wound healing that is the result of delayed epithelialization related to hyperglycemia and obesity,19,29,54 and EVs loaded with human CDK1, which shows >97% homology to mouse CDK1. This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.