When MSC-educated MDSC from healthy donors and CML patients were generated by coculturing MSC with peripheral blood-mononucleated cells, only CML-MSC-educated MDSC exhibited a suppressive ability on autologous T lymphocytes and overexpressed TGFβ, IL-6, and IL-10, thus contributing to CML immune escape [107]. The gene discussed is TGFB1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.