Another model of mouse SCD reportedly showed decreased vascular congestion and down-regulation of injury-related genes in comparison with untreated mice (the SCD model had β-globin replaced by transgenes for human βS and βS-antilles globins on a C57Bl6 background, and was treated chronically with SnPP, a short-term HO-1 inhibitor which also induces HO-1 expression over the longer term [138]). The gene discussed is HMOX1; the disease is Schnyder corneal dystrophy.