SNHG3 and congenital bilateral aplasia of vas deferens from CFTR mutation: Our previous research also found that SNHG3 is upregulated in the calcific aortic valves and acts as a decoy lncRNA, interacting with EZH2 to suppress the H3K27 tri-methylation of the BMP2 promoter, resulting in the upregulation of the BMP2 signaling pathway, thereby promoting osteogenic differentiation of valve interstitial cells in CAVD progression [27].