The fact that collagens are secreted proteins, the resemblance of COL11A1 tripeptide sequence mutants in cSCC to the dominant-negative secreted mutant COL7A1 protein seen in dominant dystrophic epidermolysis bullosa [41, 42], and the evidence above supporting engagement of integrin activation in tissue by mutant COL11A1 all raised the possibility that mutant COL11A1 secreted from tumor cells might act on adjacent COL11A1 wild-type tumor cells. The gene discussed is COL7A1; the disease is neoplasm.