The mechanism proposed by Huang and coworkers is that the secretion of interleukin-6 (IL-6) from MSCs increases the secretion of endothelin-1 (ET-1) in cancer cells, which induces the activation of Akt and ERK in endothelial cells, thereby enhancing their capacities for recruitment and angiogenesis to tumors [68]. The gene discussed is AKT1; the disease is cancer.