The evidence that in cancer models bcl-2 strongly supports the recruitment of NF-κB,33 MITF,7 Sp1,46 Hypoxia Inducible Factor 1α,5 c-Myb47 and SUFU/GLI48 at their DNA binding sites on the promoter of MMP9, TRPM1, uPAR, VEGF, Semaphorin 5A and anti-apoptotic genes respectively, indicates a general phenomenon of bcl-2 regulation in the activity of different transcription factors. The gene discussed is SEMA5A; the disease is cancer.