HU therapy, for example, has been associated with an increase in platelet-derived plasma thrombospondin-1 in SCD patients [21] and platelet-derived TNFSF14 (LIGHT) cytokine and CD40L are not significantly altered in SCA patients on HU, compared to those not on HU [19]. This evidence concerns the gene TNFSF14 and autosomal dominant cerebellar ataxia.