Furthermore, as we identified IDE-dependent but PI3Kδ-independent changes in γH2AX, which we inferred as IDE-induced chromatin modulation events, ChipSeq analysis using splenic cells from PI3Kδ-deficient/proficient mice would glean IDE drug on-target versus off-target effects; data with profound significance to CLL patients experiencing BCR drug toxicity and/or resistance. The gene discussed is BCR; the disease is B-cell chronic lymphocytic leukemia.