IFNGR1 and graft versus host disease: [11] Blockade of IFN‐γ or employment of MSCs derived from IFNγR1−/− mice demonstrated that the activation of IFNγR1 on MSCs is a prerequisite for the acquisition of the immunosuppressive capacity of MSCs.[11] In response to the dynamic changes of inflammatory factors, the immunoregulation of MSCs is highly plastic.[1] It has been reported that administration of MSCs could successfully inhibit aGvHD in the presence of vigorous inflammation such as that in steroid and cyclosporine A (CsA) resistant GvHD patients.