Malaria is a deadly human disease caused by eukaryotic parasites from the genus Plasmodium. The disease is endemic in large parts of the world putting nearly half the world’s population at risk. Plasmodium parasites infect about 250 million people every year, which resulted in 620,000 deaths in 2021. The clinical manifestations of malaria are due to the asexual growth of Plasmodium within human red blood cells (RBCs). However, the molecular mechanisms used by the parasite to transform the RBC into a suitable host are poorly understood. One reason for this is that Plasmodium parasites are deeply divergent from other well-studied eukaryotic organisms. Consequently, the molecular mechanisms driving the parasitic lifestyle of Plasmodium share little homology with well-studied model organisms. Our lab aims to unravel the molecular processes that enable P. falciparum to take over the RBC. We focus on protein secretion because this process lies at the heart of the parasite’s ability to subjugate the RBC. Establishment of infection within the human RBCs begins with parasite invasion into the host cell. Invasion is mediated by the secretion of effectors into the RBC from specialized club-shaped secretory organelles known as the rhoptry. We investigated the function of one these effectors, the Rhoptry Neck Protein 11 (RON11), which comprises of 7 transmembrane domains and a putative calcium-binding EF-hand domain. Our data show that RON11 is essential for parasite growth in the RBC. Depletion of RON11 inhibits internalization of the parasite into the host erythrocyte and using a variety of genetic, cellular as well as biochemical tools, we are uncovering the exact function of RON11 in enabling parasite invasion into human RBCs.