In turn, it is proposed that it can initiate apoptosis (by regulating and modulating the p53 protein responsible for tumour destruction, by depleting levels of Bcl-2 and Bcl-xL anti-apoptotic molecules and by interfering with the process of nuclear transcription moderated by NF-κB and AP-1 cascades) [51] and reduction of angiogenesis through inhibition of FGF-2 and VEGF, neovascularisation, as well as modulation of several signalling pathways linked to malignant progression or cell survival [52]. The gene discussed is BCL2; the disease is neoplasm.