In MS, dysautonomia and immune activation plausibly reduce endothelial NO bioavailability, augment vasoconstrictor signaling through endothelin-1 and Rho-kinase, and blunt shear-mediated vasodilation, thereby increasing resting cavernosal tone and narrowing the hemodynamic response window (Ritchie and Sullivan, 2011; Zanin-Silva et al., 2021). The gene discussed is EDN1; the disease is myeloid sarcoma.