In this issue of the Journal, 2 articles related to the phenomenon of relapse during infection with Plasmodium vivax are presented [1, 2]. Relapse is the result of the activation of quiescent liver-stage developmental forms, known as “hypnozoites,” that remain dormant within hepatocytes for varying intervals before spontaneously dividing and developing into schizonts and subsequently releasing invasive merozoites into the bloodstream to infect red blood cells. Relapse contrasts with recrudescence, which is the reappearance in peripheral blood of parasites derived from blood-stage parasites that had been at very low or undetectable levels. The timing of relapse varies with different isolates of the parasite and can be somewhat unpredictable. The development of genotyping methods has allowed for the discrimination of the primary attack parasites from the different relapse populations. On the basis of genetic similarities or differences, there has always been the question of whether the relapse parasites would possess the same genotypic pattern as the parasites responsible for the primary infection, if the primary infection resulted from the bite of a single mosquito. The 2 aforementioned articles in the current issue of the Journal, one by Imwong et al. [1] and the other by Chen et al. [2], help us to further understand the nature of this very important phase in the life cycle of the parasite.