High-throughput genomic analyses of sporadic human invasive cSCC have demonstrated the presence of frequent mutations in TGF-β receptors [3, 40, 41], indicating that TGF-β signalling is likely to act as a key tumour suppressor, and that mutational inactivation of this pathway may be a key driving event in tumour formation [3]. The gene discussed is TGFB1; the disease is neoplasm.