In fine, Bcl-xL deamidation would act both on the function and on the amount of Bcl-xL to limit its pro-survival activity; as a corollary, suppression of Bcl-xL deamidation would be another mechanism, unique to this member of the Bcl-2 family, implemented by tumor cells to acquire resistance to apoptosis. The gene discussed is BCL2L1; the disease is neoplasm.