Furthermore, a decrease in the release of multiple inflammatory cytokines, in vitro and in vivo, including IFN-γ, IP-10, IL-6, sCD40L, IL-17F, IL-1α, and LIF, similar to that shown by ruxolitinib in GVHD (35) and COVID-19 (36), also supports the ruxolitinib-mediated mechanism of synergizing with UCB-Tregs independent of IL-10 secretion in SLE. Here, CXCL10 is linked to graft versus host disease.