Consistent with the observation that malaria induces short-lived antibody responses, we recently observed that acute febrile malaria in children preferentially activates Th1-polarized PD-1+CXCR3+ Tfh (Tfh-1) cells that exhibit reduced B cell helper function [13], which is in line with several recent studies in mice showing that excessive IFN-γ suppresses germinal center B cell responses and anti-Plasmodium humoral immunity [14–17]. The gene discussed is IFNG; the disease is malaria.