In the present study, we found that ox-LDL upregulated miR-17∼92a cluster expression and increased the number of new proliferations of VSMCs, AD treatment resulted in a significant reduction of miR-17∼92a expression, and the capacity of proliferation in ox-LDL-induced VSMCs was markedly inhibited following the treatment with AD. It has been recently confirmed that the miR-17∼92a cluster are mediated by the ERK pathway in endothelial cells [16] and miR-18a promotes cell proliferation via AKT and ERK pathways [31]. Here, AKT1 is linked to Alzheimer disease.