The main mechanism of Acute Coronary Syndrome (ACS) has been thought to be thrombus formation accompanying the rupture of coronary atheroma (plaque). However, in the present day when Low-Density Lipoprotein (LDL) cholesterol can be reduced by HMG-CoA reductase inhibitors (statins), thrombosis due to “erosion” and not rupture of plaques is attracting attention as an important mechanism of ACS. ACS due to eroded plaques involves inflammation and immunity, particularly Neutrophil Extracellular Traps (NETs). Therefore, it is necessary to reevaluate whether invasive treatments and antithrombotic therapy that have been used for ACS due to plaque rupture are most suitable and to investigate new personalized treatments. In the future, personalized treatments corresponding to different mechanisms of ACS should be investigated and drugs that inhibit the formation of NETs may become a treatment option.