During this time of continued ibrutinib therapy, CLL cells are deprived of tissue-based microenvironmental stimuli, and proapoptotic and autophagocytic mechanisms kick on: CLL cells increase expression of proapoptotic BimEL, and LC3B-II promotes autophagocytosis while shrinking in size and downmodulating expression of the majority of surface receptors, including sIgD [66]. The gene discussed is BCL2L11; the disease is B-cell chronic lymphocytic leukemia.