As soon as precise markers of severity are available, it would be possible to design studies powered to analyse the influence of the host genetics in the development of severe vivax disease. Some association between pulmonary manifestations and TNF and IL-12 polymorphisms has been attempted [79] . It has been proposed for the first time in Manaus that G6PD deficiency could protect against vivax malaria, in a cross-sectional study, based on past history of the enrolled population [149] . This protection was later confirmed in Pakistan [150] . Male hemizygotes for this deficiency also showed to be protected against severe falciparum malaria [151] . No data exist on the protection against severe vivax disease. Likewise, people with the FYA/FYB genotype presented higher susceptibility to clinical vivax malaria [152] . Since the discovery in Brazil that Duffy-negative individuals could be infected by P. vivax [153] , some speculation on the other possible invasion receptors has emerged. However, cohort studies are needed to investigate the real impact of the distinct Duffy genotypes on clinical malaria incidence, submicroscopic asymptomatic infection, malaria-triggered anaemia and lower parasitaemia, as already suggested for FYB/FYX and FYA/FYX genotypes in the Brazilian Amazon [154] .