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Multiple studies have shown that the rodent parasite evades this defense by recruiting the C-type lectins CTL4 and CTLMA2, while permissiveness to the human malaria parasite was not affected by partial depletion of these factors by RNAi silencing. Using CRISPR\/Cas9-based CTL4 knockout, we show that <jats:italic>A<\/jats:italic>. <jats:italic>gambiae<\/jats:italic> can mount melanization-based refractoriness to the human malaria parasite, which is independent of the TEP1 complement-like system and the major anti-<jats:italic>Plasmodium<\/jats:italic> immune pathway Imd. 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