Thrombophilia associated with vWF, FVIII, and FV is the result of an impaired turnover of these proteins, which favors the factors’ synthesis, due to an alteration in natural inactivators, such as ADAMTS13 for vWF [270] (Figure 3) and APC and PS for FVIII (Figure 4) and FV (Figure 5), respectively [268,269]. This evidence concerns the gene PRB2 and thrombophilia.