Persistent STAT3 activation promotes the growth and survival of tumor cells through modulation of cell cycle regulators (e.g., cyclin D1/D2 and c-Myc), upregulation of anti-apoptotic proteins (e.g., Mcl-1, Bcl-xl, and survivin), downregulation of the tumor suppressor p53, and induction of angiogenesis by vascular endothelial growth factor (VEGF); these mechanisms eventually contribute to tumor progression and resistance to anti-cancer drugs [6, 8, 9]. Here, BCL2L1 is linked to neoplasm.