Thus, if documented systemic excess CO generation by heme oxygenase-1 did not play a role in the hypercoagulation caused by diverse inflammatory states (e.g., cancer, obesity, dialysis, migraine headache), then some other common, pathological biochemical modification of fibrinogen must have occurred that rendered fibrinogen no longer responsive to CORM-2 modulation. The gene discussed is HMOX1; the disease is cancer.