(83) verified that miR-30e could exert an inhibitory effect on the proliferation and migration of human VSMCs and act as an antiatherosclerotic agent by negatively targeting Ube2i and reducing the IκBα/NFκB signaling pathway in rats in vivo. Similarly, lincRNA-p21 functioned as a negative regulator of VSMC proliferation during atherosclerosis and induced VSMC apoptosis by directly binding to the E3 ubiquitin ligase MDM2, decreasing MDM2-p53 interactions and ubiquitination degradation, ultimately promoting p53 activity in mice in vivo and in vitro (84). This evidence concerns the gene NFKB1 and atherosclerosis.