In the context of sepsis, there is initially a disturbance in hemodynamics, as there is a disproportional increase in NO formation, primarily due to the increased induction of NO synthase (iNOS) via NFκB, but also due to cyclooxygenase-2 (COX-2) expression, leading to generalized vasoplegia, which is compensated for by increased activation of the sympathetic nervous system with the release of noradrenaline and adrenaline. The gene discussed is PTGS2; the disease is Sepsis.