This is evidenced by the exceptional clinical efficacy of inhibitors targeting BCR signaling, such as ibrutinib (Bruton’s tyrosine kinase (BTK) inhibitor) or idelalisib (Phosphatidylinositol 3-kinase (PI3K) inhibitor), in reversing the CLL disease phenotype suggests an enormous importance of BCR-derived survival signals for CLL cell persistence (15–18). The gene discussed is BTK; the disease is B-cell chronic lymphocytic leukemia.