A recent study by Nasser et al. [34] divided hypercoagulability into two categories: Type I occurs when there is an imbalance between endogenous heparin production and its degradation by an enzyme called heparanase and Type II includes hypercoagulability caused by factors such as stasis, treatment, poor performance status etc. The role of heparanase in CAT has been verified by a series of studies, most of which have concluded that heparanase expression is associated with oncogene expression, including RAS mutations [35,36,37,38]. Here, HPSE is linked to thrombophilia.