In vitro experiments demonstrated that Lp(a) and its oxidized phospholipids induce pro-osteogenic changes in valve interstitial cells through an inflammatory pathway involving nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and bone morphogenetic protein 2 (BMP2) [14]. inhibition of autotaxin or blocking its Lp(a) receptor could be promising therapeutic strategies for aortic valve disease, warranting further investigation. This evidence concerns the gene BMP2 and aortic valve disorder.