PLCG2 and B-cell chronic lymphocytic leukemia: Figure 9C shows that the disease-related PLCγ2 point mutants showed marked differences in their activities, but that none of them reached the high activity of PLCγ2ΔSH, which was still 4.2-fold higher (based on the amounts of cDNA required for half-maximal inositol phosphate formation) than the activity of PLCγ2R665W|L845F|S707Y, the most active of the point mutants mediating ibrutinib resistance in CLL patients.