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. This evidence concerns the gene ZFP36 and psoriasis.