tRNAs are not only essential for decoding the genetic code, but their abundance also has a strong impact on the rate of protein production, folding, and on the stability of their encoding messenger RNAs. Plasmodium expresses a unique surface protein called tRip, involved in the import of exogenous tRNAs into the parasite. Comparative proteomic analysis of the blood stage of wild-type and tRip-KO variant of P. berghei parasites revealed that down-regulated proteins in the mutant parasite are distinguished by a bias in their asparagine content. We therefore propose a model in which a dynamic import of host tRNAAsn allows the synthesis of asparagine-rich regulatory proteins that efficiently and selectively control the parasite infectivity. These results suggest a novel mechanism of translational control where import of host tRNAs emerge as critical regulator of gene expression in the Plasmodium developmental cycle and pathogenesis.