The essential role of CXCR4 in T-ALL pathogenesis was recently demonstrated in a NOTCH1-induced T-ALL mouse model [194], where inhibition of endogenous CXCR4 expression by short hairpin RNA (shRNA) impaired CXCL12-induced migratory properties of T-ALL cells, and also induced cell death and altered cell cycle progression in vitro. The gene discussed is CXCR4; the disease is acute lymphoblastic leukemia.