As has been discussed above in more detail in the section on CCN2 and ALL, the EXM-BM derived from CCN2 knockdown MSCs proved to be more adipocyte-rich, which can be attributed to the inhibitory effect of CCN2 on the adipogenic differentiation of MSCs, and expressed higher levels of leptin and CXCL12 than the EXM-BM derived from normal MSCs (Battula et al. 2013). The gene discussed is CCN2; the disease is acute lymphoblastic leukemia.