To validate these results and assess the potential functionality of PLCγ2 in B-ALL, we performed Ca2+ signaling experiments in the absence of extracellular Ca2+, in order to mobilize only the ER Ca2+ stores via the IP3 receptor (IP3R), which is a hallmark of PLCγ2 activation. This evidence concerns the gene ITPR3 and precursor B-cell acute lymphoblastic leukemia.