Apart from its pro-apoptotic, growth inhibitory, and anti-angiogenic properties (Keyes et al, 2002; Graff et al, 2005; Querfeld et al, 2006; Willey et al, 2009), this could be, at least in part, due to downregulating tumour progression and invasion-related genes (u-PAR, HIF1α, and VEGFC) and upregulating NSCLC tumour-related suppressor genes (FHIT, RASSF1, and VHL) by Enz. The gene discussed is FHIT; the disease is neoplasm.