There are several mechanisms that prevent excess clotting.
One of these mechanisms is to inactivate factor Va. Normally, factor Va is inactivated when it is cleaved by a complex that includes activated protein C (APC), protein S and thrombomodulin.

One cause of an increased likelihood of blood clots is a common variant of the gene that encodes factor V (factor V is the precursor to factor Va). This variant, factor V-Leiden, has an amino acid substitution that slows its inactivation rate by about 80-fold.
About 10% of those with Factor V-Leiden will develop thrombophlebitis.
About 5% of the U.S. population is heterozygous for factor V-Leiden.

Mutations in protein C or protein S also increase the chance of thrombophlebitis and are fairly common (about 1/200 - 1/500). Mutations in thrombomodulin are much less common.