This proposed role is supported by evidence from three human “models” of squamous skin tumours: a clear genotype-phenotype correlation between germline inactivating TGFBR1 mutations and families suffering from multiple self-healing squamous epithelioma (MSSE) [42], the presence of TGFBR1 mutations in sorafenib-induced skin tumours [43] and clinical cancer trial data reporting spontaneous cSCC arising as a side-effect of systemic treatment with the pan-TGF-β ligand antibody, GC1008 [44]. This evidence concerns the gene TGFBR1 and skin neoplasm.