In LGL leukemia, the pro-/anti-apoptotic balance is impaired in favor of increased resistance to cell death by neoplastic clones, also mediated by enhanced phosphoinositide 3-kinase (PI3K)/Akt signaling pathway activation through RANTES (also known as chemokine (C-C motif) ligand 5 or CCL5), IL-18, and macrophage inflammatory protein (MIP)-1b stimulation [33,39]. The gene discussed is CCL5; the disease is T-cell large granular lymphocyte leukemia.