Bax drives to apoptosome formation and caspase-3 activation, promoting apoptosis and has been reported that Bcl-xL, encoded by BCL2L1 (BCL2-like 1) gene [11], is able to stabilize the mitochondrial localization of Bax, maintaining it in an inactive state [12], which is a mechanism implicated in cell survival in different tumor types [13]. This evidence concerns the gene BCL2L1 and neoplasm.