It is possible thanks to n3 PUFAs ability to change the balance between pro- and antiapoptotic activity of Bcl-2 protein in favor of cancer cell death [55], thanks to EPA ability to suppress cell division through translation initiation suppression [56], thanks to the mechanisms of attenuation of wasting by n-3 PUFA centre largely around catabolic signal transduction by cytokines, eicosanoids and tumour-derived proteolysis-inducing factor [57], through antiangiogenic [58] and antimetastatic [59] activity of n3 PUFAs. The gene discussed is BCL2; the disease is neoplasm.