Blockadeof exosomal uptake from keratinocytes impaired wound closure withthe persistence of proinflammatory mφ in the wound microenvironment,pointing toward a bidirectional crosstalk between these two cell types.The significance of such bidirectional crosstalk was established bythe observation that in patients with nonhealing diabetic foot ulcers,TOMM70 is deficient in keratinocytes of wound-edge tissues. The gene discussed is TOMM70; the disease is diabetic foot.