Parasitic infections affect nearly 1 in 6 people worldwide. These infections thrive when parasites are able to evade, inhibit, or disrupt host defense mechanisms. One way parasites avoid the immune response is to disguise themselves as dying host cells. Normal host cells undergoing apoptosis expose a molecule called phosphatidylserine (PS) on the plasma membrane as a signal to surrounding cells. This signal is detected by phagocytic immune cells, which engulf the dying cell and reduce inflammation. The system is co-opted by parasites, who use PS as a Trojan horse to enter phagocytic immune cells, infecting the host. This process, known as “apoptotic mimicry, ”takes several forms. Classical apoptotic mimicry - where the PS comes from the challenger - is used by the parasites that cause leishmaniasis, American trypanosomiasis, and toxoplasmosis; while non-classical apoptotic mimicry, which co-opts PS exposed by dying host cells, is used by the parasites that cause malaria and amebiasis. Better understanding these mechanisms will help researchers identify ways to block parasitic entry and boost the immune response, paving the way for innovative therapeutic strategies to fight parasite infection.