Of relevance, earlier, we have shown that CLL cells express AXL as a constitutively active receptor tyrosine kinase (RTK), albeit at differential levels, and acts as a docking site of multiple signal mediators including PI3K/AKT, Lyn, SYK/ZAP70 and phospholipase C (PLC)γ2, regulating CLL cell survival20,21. This evidence concerns the gene AKT1 and B-cell chronic lymphocytic leukemia.