A potential explanation might be that exosomal miR-186-5p might modulate the LOX-1 and SHIP2-mediated PI3K/AKT/mTOR pathways to facilitate lipid accumulation and promote viability and invasion in VSMCs, thereby contributing to atherosclerosis, which led to the occurrence of AMI (15, 17). The gene discussed is INPPL1; the disease is atherosclerosis.