There are many possible explanations for the partial efficiency of BH3 mimetics, including cancer heterogeneity, the lack on specific BH3-mimetics optimized for the different BCL2 members governing cell death resistance in the tumor, and mutations or posttranslational modification in the BCL2 family members that alter their canonical function and structure [45,49,55]. The gene discussed is BCL2; the disease is neoplasm.