The BTK inhibitor ibrutinib abrogated IL-10 and CSF1 production, the latter of which was achieved by targeting the BCR signaling network, in MCL cells, leading to inhibition of CD163+ polarization of the ibrutinib-sensitive MCL cells, thereby, suppressing M2-like macrophage-dependent MCL pro-survival and proliferative effects. This evidence concerns the gene CSF1 and mantle cell lymphoma.