Importantly, calcitriol/VDR signaling capacity was maintained in CLL cells under ibrutinib since calcitriol administration to ibrutinib-treated cells could upregulate CYP24A1 and pERK and decrease pNF-κB, further supporting our argument that microenvironmental signaling does not impede calcitriol action. This evidence concerns the gene EIF2AK3 and B-cell chronic lymphocytic leukemia.