Upon antigen stimulation, BCR signalling induces LYN and SYK phosphorylation (P in orange circles refer to phosphorylation) that initiate a signalling cascade causing downstream BTK activation. BTK is recruited into the signalling complex at the plasma membrane via the docking of its pleckstrin homology domain to phosphatidylinositol 3,4,5 triphosphate (PIP3). BTK becomes phosphorylated and therefore induces calcium release, which initiates a signalling cascade with the consequent induction of cell proliferation and survival. BTK is also involved in signalling of chemokine receptor CXCR4, which is important in cell migration and could be a suitable target for ibrutinib.