Next, we compared the effects of PLCG2 mutations observed in ibrutinib-resistant CLL patients to a PLCG2 deletion, ΔSH, effectively removing the entire autoinhibitory nSH2-cSH2-SH3 region of the encoded protein and previously characterized as one of the most active deletion mutant of PLCγ [16, 25]. The gene discussed is PLCG2; the disease is B-cell chronic lymphocytic leukemia.