Three observations suggested alterations in circulating CLL platelets: a decrease in platelet granularity/complexity, an ibrutinib-independent decrease in membrane levels of αIIbβ3 and GPVI compared to controls, and a reduction in lag time for onset of platelet aggregation in response to bacteria; although the latter could also be due to changes in plasma composition in CLL. This evidence concerns the gene GP6 and B-cell chronic lymphocytic leukemia.