However, it is possible (or even plausible) that tumor microenvironment can provide diverse pro-survival stimuli that increase survival of lymphoma cells under in vivo hypoxia, including upregulation of anti-apoptotic molecules (e.g., BCL-XL), or activation of several key prosurvival signaling pathways (e.g., PI3K-AKT) [4]. Here, BCL2L1 is linked to neoplasm.