Our previous work demonstrated that in inflammation-mediated spontaneous abortion models, treatment with MSCs inhibited the proliferation of CD4+ T cells by inducing the decidual macrophage switch to the M2 phenotype, which led to the abortion relief.6 In addition, MSCs also exert direct effects on T cells through the production of immunosuppressive molecules, such as NO, indoleamine 2,3-dioxygenase, prostaglandin E2, transforming growth factor β (TGFβ), heme oxygenase 1, and leukemia inhibitory factor. The gene discussed is HMOX1; the disease is abortion.