The human malaria parasite Plasmodium falciparum invades and reproduces inside human red blood cells. To ensure its own survival, the parasite modifies its host cells biochemical and biophysical properties. Host cell modifications are mediated by proteins that are exported from the parasite inside the red blood cells. For example, these proteins induce the generation of small protrusions on the surface of infected red blood cells, so called knobs, which allow binding and cytoadhesion to endothelial receptors and thus escaping from splenic clearance. In the recent decades, many exported proteins have been already successfully characterized. However, due to technical limitations and the haploid nature of blood-stage parasites, some highly interesting protein candidates have yet to be characterized. In my PhD project, I am using new genetic tools to investigate so far uncharacterized exported proteins that are likely essential for host cell modification and the intra-erythrocytic survival of P. falciparum. Therefore, I am generating conditional knockout cell lines using CRISPR-Cas technology and the DiCre recombinase. I will then characterize these knockout cell lines in different aspects of parasite growth and development, host cell modification and especially knob formation, cytoadherence and the localization of other exported proteins. The long-term goal of my project is to understand the mechanisms and identify the proteins involved in parasite-induced host cell modification, with a view to target these in the future as potential anti-malarial drugs.