**7. Conclusion**

From the point of view of molecular biology and its defects in the development of different diseases, this chapter explores the mechanism of efferocytosis. Just a few examples of the potential effect of disrupted efferocytosis on human diseases are cancer, autoimmune diseases, lung inflammation and atherosclerosis. However, impaired clearance of apoptotic cells, including neurodegeneration, skeletal alterations, cardiac growth, electrical impulse propagation and post-injury recovery, angiogenesis and wound healing, is believed to be involved in many other diseases with unfavorable prognosis and processes. In general, in an inflammation-silenced environment, efferocytosis involves many cells and molecular steps leading to the removal of apoptotic cells. Find-me and eat-me signals are secreted by apoptotic cells for this function, while phagocytic cells often work to clear apoptotic debris with the aid of bridging molecules. Anti-inflammatory interleukins are secreted after the engulfment of apoptotic cells. In fact, cancer progression can be increased by both defective and enhanced efferocytosis. Overall, it is possible to inhibit or activate the receptors associated with this process with accurate knowledge of the molecular mechanisms involved in the efferocytosis process and to target strongly for a new window in the treatment of many human diseases.
