The mutation causes overproduction of an enzyme that accelerates blood clot breakdown.

A person prone to abnormal clotting has an imbalance between clot formation and clot breakdown.

As an enzyme, it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown.

The degree and extent of symptoms depend on the size and location of the obstruction, the occurrence of clot fragmentation with embolism to smaller vessels, and the degree of peripheral arterial disease (PAD).