All effects of MSCs in solid tumors can be explained by two mechanisms: 1) differentiation of the multipotent MSCs into tumor-associated tissue elements such as fibroblasts [12], tumor-associated blood vessel endothelium [5] and/or smooth muscle [13] or 2) MSCs are not stably associated with these sites, rather they affect tumorigenesis via producing various angiogenic (VEGF, PDGF, FGF) [4], immunosuppressive (TGF-β1, IDO, IL-10, PGE2) [14] and metastatic (CCL5) [15], [16] factors. The gene discussed is VEGFA; the disease is neoplasm.