The capacity of REG3A to control TLR3-induced inflammation and its effect on keratinocyte proliferation are critical, but irreplaceable, for normal wound healing responses in diabetes, as SHP-1silencing in vitro did not inhibit keratinocyte proliferation induced by REG3A itself (Supplementary Fig. 9), and the inactivation of SHP-1 by SSG in vivo only partially inhibited RegIIIγ-promoted wound healing in diabetes. The gene discussed is NR0B2; the disease is diabetes mellitus.