Different death-styles have been described in unicellular organisms. In most cases they evolve with phenotypic features similar to apoptotic death of animal cells, such as phosphatidylserine (PS) exposure, oligonucleosomal DNA fragmentation, and loss of mitochondrial transmembrane potential, hinting that similar mechanisms operate in both situations. However, the biochemical pathways underlying death in unicellular organisms are still unclear. Host recognition of PS exposed on the surface of unicellular parasites is an important feature of the process of infection and progression of the disease. Here, we discuss data showing that entirely different mechanisms of PS exposure co-exist during the life-cycle of Leishmania amazonensis: in the case of promastigotes, a sub-population dies by apoptosis; in the case of amastigotes, the entire population exposes PS, not necessarily followed by apoptotic death. This phenomenon has been called apoptotic mimicry. The elusive caspase-like activities described in protozoa are also discussed.