Wang et al. (2019a) demonstrated that MALAT1 has a direct impact on autophagy; in the HUVEC model of atherosclerosis, this lncRNA sponges miR-216a-5p to positively regulate BECLIN1 and promote autophagy (Wang et al., 2019b). Moreover, MALAT1 contributes to atherosclerosis by inhibiting autophagy in the endothelial progenitor cells via miR-15b-5p/MAPK1. Mitogen-activated protein kinase 1 (MAPK1), whose expression is associated with atherosclerosis, can activate the mTOR signaling pathway to inhibit autophagy (Zhu et al., 2019). Here, MTOR is linked to atherosclerosis.