Hence, we tested the effect of heterozygosity for the known loss of function mutation at murine Pklr (G338D) [50], on haematological replication of the malarial parasite in a mouse model of infection with P. chabaudi. For this, wild-type controls (CBA/CaHn-Btkxid/J), pyruvate kinase deficient mutants (CBA/Pkslc) homozygous for a loss of function allele at Pklr (G338D), as well as F1 heterozygotes (G338D/+) were infected with P. chabaudi AS and blood parasitemia was followed over time (Fig 3C). This evidence concerns the gene PKLR and infection.