Our study results showed that low expression of lnc-MICALL2-2 enhanced HCAECs proliferation and suppressed HCAECs apoptosis in an oxLDL-induced model of early CHD, which suggested that the knockdown of lnc-MICALL2-2 may become a future therapeutic approach for oxLDL-related CHD. This evidence concerns the gene MICALL2 and coronary artery disorder.