Although the complete molecular pathways in which the genetic variants predispose people to cardiovascular disease are still unknown, recently several possible mechanisms have been proposed; for instance, it has been postulated that phosphatase regulation plays a specific role in CAD pathophysiology, through protein phosphatase and actin regulator 1 (PHACTR1), a molecule that inhibits protein phosphatase-1 (PP1) and binds actin via the C-terminal domain [8]. Here, PHACTR1 is linked to cardiovascular disorder.