Inflammatory response plays an important part in the formation and progression of vulnerable plaque. It regulates the lesions locally in the artery as well as the global inflammatory status. Some pro-inflammatory cells and cytokines can reduce the tensile strength of the collagen cap surrounding the plaque and enlarge the necrotic lipid core, thus causing the loss of mechanical stability and plaque rupture. On the other hand, activation of inflammatory response and metabolic disturbance can also instigate endothelial dysfunction, plaque erosion, and further thrombosis. Such process is mediated by several immune cells such as macrophages and lymphocytes, along with other regulatory factors consisting of cholesterol crystals and lipid mediators, shear stress as well as angiogenesis and intraplaque haemorrhage. Moreover, several anti-inflammatory factors are found able to protect the vulnerable plaque from rupture or erosion, highlighting the balance of inflammatory response is essential for the occurrence of acute coronary syndrome (ACS). Thus, targeting specific factors in the inflammatory response may be valuable in screening and treating patients with vulnerable plaque, preventing ACS and improving the prognosis.