In one study, the forced or regulatory expression of the anti-apoptotic Bcl-2 or c-Myb proto-oncogene product’s transcription factor participates, transcriptionally and translationally, in sustaining increased levels of Sema5A and contributes to the progression of melanoma, which is derived from cells in the skin called melanocytes, from neural crest cells [41]. The gene discussed is BCL2; the disease is melanoma.