Hypoxia-inducible factor 1α, one of the essential targets of Enz validated in this study, is getting stabilised in hypoxic conditions, inactivates tumour-suppressors (p53, PTEN), activates several oncogenic pathways (Src, HER/2, H-ras) (Zhang et al, 2007), and transactivates VEGF through hypoxia response elements, this being central to the initiation of pro-angiogenic signalling and neovascular formation (Forsythe et al, 1996). The gene discussed is TP53; the disease is neoplasm.