This same NK-1R antagonist is known to promote apoptosis in many other tumor cells [4] and the blockade of this receptor by L-733,060 caused the cleavage of caspase-3 and the proteolysis of poly (ADP-ribose) polymerase, increased apoptosis and inhibited the basal kinase activity of Akt [57]. The gene discussed is AKT1; the disease is neoplasm.