Several other studies demonstrated that, in human primary chronic lymphocytic leukemia (CLL) cells, ibrutinib is able to not only cause apoptosis through activation of caspase 3 but also block CLL cell proliferation via suppression of BCR- and CD40-activated Akt, ERK, and NF-κB pathways, all of which are downstream targets of BTK [50]. This evidence concerns the gene AKT1 and B-cell chronic lymphocytic leukemia.