In addition, in a global transcriptional analysis of SCA patients, HO-1 and its by-products were upregulated in circulating blood mononuclear cells together with genes involved in heme metabolism, cell-cycle regulation, antioxidant and stress responses, inflammation and angiogenesis [130], which suggests that circulating mononuclear cells could participate in compensating for sickle cell vascular injury. The gene discussed is HMOX1; the disease is autosomal dominant cerebellar ataxia.