Leishmania are protozoan parasites that infect various mammalian species, including humans. It is generally thought that random attachment of the flagellated promastigotes to mononuclear phagocytes initiates their uptake via circumferential pseudopods. Intracellularly, the promastigotes become located in phagolysosomes in which they transform to and survive as ‘aflagellated' amastigotes that hide their shortened flagellum within the flagellar pocket. Unrestricted replication of these amastigotes is assumed to cause the eventual burst of the host cell, thereby releasing the infectious parasites. Here, Mike Rittig and Christian Bogdan review a large body of literature containing potentially important but poorly appreciated findings, which together with recent results, argue for Leishmania–host-cell interactions that are much more complex than generally thought.