Inhibition of BTK by ibrutinib or knockdown of BTK by siRNA in primary AML cells and AML cell lines decreases NF-κB survival pathways, SCF-CD117-BTK-MAPK/ATK signaling, G-CSFR mutants-BTK signaling, FLT3-ITD-BTK-NF-κB/MAPK/AKT/STAT5 signaling, and SDF1/CXCR4-BTK-AKT/MAPK signaling, leading to reduced cell survival and proliferation as well as migration (43–48). The gene discussed is CXCL12; the disease is acute myeloid leukemia.