For example, Gs hyperfunction leads to an enhanced tendency for bleeding,100 enhanced NO signaling correlates with reduced risk of thrombosis,101 whereas Gs or sGC dysfunction culminates in enhanced susceptibility to thrombosis.60, 102 In particular, loss of sGC expression, through a combination of mutations in the α1 subunit of sGC and in the sGC‐interacting chaperone CCTη, was shown to reduce platelet cGMP levels and to increase the risk of myocardial infarction.60 Recently, a meta‐analysis identified PDE3A as a novel stroke risk locus.103. Here, SGCB is linked to myocardial infarction.