Unlike, the known involvement of canonical p65-dependent NFκB transcriptional activity in the growth of UVB-induced SCCs [98, 101], we show here enhancement of Bcl3-regulated non-canonical NFκB signaling in BCCs; furthermore we also found similar nuclear localization of the p50-Bcl3 complex in BCCs from patients with NBCCS. This evidence concerns the gene BCL3 and nevoid basal cell carcinoma syndrome.