When introducing the term "hypnozoite" in the late 1970s, I (like others at the time) theorized that hypnozoites trigger malarial relapses. This concept has since become transmogrified into a "fact", albeit unproven in humans. Nevertheless, the indirect evidence for the validity of the hypothesis is compelling, and it is almost certainly correct, as far as it goes. A confounding factor in some situations, however, is that the (probable) anti-hypnozoite drug primaquine also has merozoitocidal effects; and it is not known whether primaquine can effectively kill Plasmodium vivax parasites in all of their habitats in the body. There is little-known evidence that it might not do so. Associated interpretational difficulties in respect of the individual patient aside, I now believe that many of the genotypically homologous, non-reinfection recurrences that researchers ascribe to hypnozoite activation are, in fact, hypnozoite-independent (some malariologists are starting to agree). Thus, they are recrudescences (not relapses). Since 2010, there has been speculation as to whether quiescent P. vivax merozoites occur in extra-erythrocytic sites, such as in splenic dendritic cells, to name but one possible site. A recent suggestion is that blood-stage merozoites in the bone marrow might be a source of or contribute to homologous (specifically) P. vivax malarial recurrences. The latest concepts concerning the biology of P. vivax recurrences (Markus, 2017, 2018) will be presented. If hidden, non-hypnozoite parasite forms do facilitate ongoing transmission of P. vivax malaria, then they are collectively (like hypnozoites, probably) an obstacle to eradication of the disease. REFERENCES: Markus, M.B. 2017. Malaria eradication and the hidden parasite reservoir. Trends in Parasitology 33: 492-495; Markus, M.B. 2018. Biological concepts in recurrent Plasmodium vivax malaria. Parasitology (In Press for Special Issue): https://doi.org/10.1017/S003118201800032X