This finding may be of clinical relevance, as NO-independent stimulators and activators of sGC are being developed for use in diseases, including pulmonary hypertension (Mittendorf et al., 2009), in which NO signaling is reduced or absent (Rabinovitch, 2007; Stasch and Evgenov, 2013) and, as we have shown, TSP1-CD47 signaling concurrently upregulated (Bauer et al., 2012). The gene discussed is SGCB; the disease is pulmonary hypertension.