Although PfEMP1/var is studied in many laboratories in the world, a number of key questions remain unknown. By analysing a mutant parasite (D10) with a chromosome 9 deletion and loss of adhesion, we linked the non-cytoadherence phenotype to the loss of 25 subtelomeric genes. However, in contrast to previous publications, knockout of the clag9 gene from 3D7 did not interfere with parasite adhesion to CD36. In addition, we demonstrate for the first time the surface expression of PfEMP1 that has lost binding to receptors but is still recognized strongly by human hyperimmune serum similar to infected RBC that cytoadhere (Nacer et al., 2011 PLoS One). By carefully analysing the genes deleted on chromosome 9 of D10, 12 genes were selected as possible candidates and used for episomal complementation studies of D10. One single gene annotated as an open reading frame with no obvious homology to any known gene was able to restore adhesion. We termed this gene PfVAP1 (Virulence Associated Protein 1). To further validate this finding, an inducible protein knock down of the PfVAP1 gene was obtained for the strongly cytoadherent reference line FCR3. In conditions of reduced expression of PfVAP1, FCR3 parasite adhesion is to at least 60 to 70% (Nacer et al., 2015 Cell Microbiol). According to the Plasmodium databank PlasmoDB (www.plasmodb.org), PfVAP1 seems to be highly expressed during the gametocytogenesis, the parasite development process to form gametocytes. Thus, it seems important to investigate the PfVAP1 expression in the sexual stages. Further analysis of PfVAP1 is ongoing to investigate it’s biological role in this adhesion process.