However, considering that individuals homozygous for haplotype A (thus carrying the ‘inhibitory’ KIR genotype A/A) produced significantly less IFN-γ in response to stimulation with P. falciparum antigens (14) it is plausible too that the predominance of activating KIRs (or the relative absence of inhibitory KIRs) contributes to exacerbated inflammatory responses that have been implicated repeatedly in the pathogenesis of severe malaria (13, 56). The gene discussed is KIR3DL1; the disease is malaria.