According to ‘the response to injury’ theory of atherosclerosis, the entry of monocytes into the intima guided by inflammation signals, taking up cholesterol and transforming into foam cells, and egress from plaques, determine the progression of atherosclerosis. Foam cells can migrate out of the plaque through certain mechanisms, and this process determines the development or regression of the plaque. So far, the research on the mechanism of monocyte migration has mainly focused on cytokines/receptors. Multiple cytokines and receptors have been reported to be involved in monocytes recruitment such as CCL2/CCR2, CCL5/CCR5, and CX3CL1/CX3CR1, and the egress of macrophages from the plaque like CCR7/CCL19/CCL21.In addition, some neural guidance molecules such as Netrin-1 and semaphorin 3E, have an inhibitory effect on monocyte migration. However, the entry and egress of monocytes from plaques is a complex biomechanical process regulated by chemokines. Biomechaincal studies on biomechanical property alteration of monocytes in the process of entry and egress from plaques will be helpful in uncovering the specific mechanical process of the occurrence and development of atherosclerosis and seeking potential therapeutic approaches for atherosclerosis recovery from biomechanical perspective.