Since C7 is not a classical tumor suppressor (patients heterozygous for COL7A1 mutation are not at increased risk of developing cancer, and COL7A1 mutation has not been associated with any non-RDEB cancer to date), the incidence of SCC in RDEB seems not to be driven by cell-intrinsic effects of mutation in COL7A1 but rather extrinsic effects of lack of C7. This evidence concerns the gene COL7A1 and neoplasm.