Nitric oxide production is reduced because of an impaired vascular endothelial growth factor pathway, mediated through the MAPK pathway.29 The upregulation of cluster of differentiation 47 induced by BRAF and MEK inhibition also inhibits the signaling of nitric oxide–cyclic guanosine monophosphate, reduces nitric oxide bioavailability, and thus contributes to recurrent vasoconstriction, hypertension, and an imbalance between thrombotic and antithrombotic states.30,31 This could serve as an explanation for the occurrence of pulmonary embolism and myocardial infarction. This evidence concerns the gene BRAF and hypertensive disorder.