Additionally, it was found that IMM-H007 and recombinant BSCL2 could reduce aortic valve calcification both in vitro and in vivo.<h4>Conclusion</h4>We identified that an oxLDL-induced transcription factor FOXS1 inhibits ABCA1 and ABCG1 expression via the BSCL2/PPARγ/LXRα axis and promotes cholesterol transport dysfunction and the activation of NLRP3 inflammasome in VICs, thereby accelerating the progression of CAVD. The gene discussed is ABCA1; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.