In addition, more studies are needed to understand how Candida influences its recognition in vivo by employing immune evasion strategies; for example, β-glucan exposure on the Candida surface occurs in infected mouse tissues only late after infection [14], thus preventing CLR-mediated pathogen recognition during the early phase of invasive infection, when recruitment of effector immune cells is critical for survival [15]. This evidence concerns the gene DCLK3 and infection.