FERMT1 and Kindler syndrome: Studies in clinical samples support a role for TGF-β signaling and stromal fibroblasts in promoting a pro-tumorigenic environment in KS patients [17, 18], while links to UV exposure and inflammation have also been made [12], with reports of upregulation of proinflammatory cytokines in Kindlin-1-deficient keratinocytes [18–20].