Signaling through the BCR propagates via phosphorylation of downstream mediators, eventually resulting in constitutive activation of signaling pathways -such as NF-κB, JAK/STAT, and MAPK- that sustain leukemia cell viability by, at least in part, upregulating the expression of antiapoptotic members of the BCL2 family of proteins (44). Here, SOAT1 is linked to leukemia.