Current hypotheses that have been postulated to explain the inhibition of tumor angiogenesis by hMSCs include promotion of endothelial cell apoptosis [50], modulation of the VE-cadherin/beta-catenin pathway [39, 40], and suppression of vascular endothelial growth factor (VEGF) expression [43]. The gene discussed is CTNNB1; the disease is neoplasm.