ZFP36 and multiple sclerosis: We have previously demonstrated that increased stability of TTP can confer protection against inflammatory responses in various mouse models of human disease, including RA, psoriasis, multiple sclerosis, and others [2, 13] but it is unclear how the increased TTP affects the early hematopoietic progenitor compartment, and whether the mitigation of inflammation is exclusively driven by the hematopoietic compartment.