The amelioration of the TTP deficiency syndrome by a gene deletion (i.e., Il23, Ccl3, Tnfr1) or antibody-mediated neutralization of a TTP target (i.e., anti-TNF-α antibodies) in TTP−/− mice is regarded as an important evidence for a causal role of the particular gene in development of the TTP phenotype (23, 24, 41, 47). Here, CCL3 is linked to thrombotic thrombocytopenic purpura.