Malaria is a vector-borne disease caused by several unicellular Plasmodium species. Plasmodium are parasitic eukaryotic protozoans within the apicomplexan phylum named for an apical complex of secretory organelles and cytoskeletal components critical for host cell invasion. Infections are deadliest in children under five years of age and pregnant women. Here, we focus on the life cycle of Plasmodium falciparum and the molecular remodeling capabilities implemented against human erythrocytes. These changes can complicate Malaria infections and reach the microvasculature of the brain leading to death in the human host. Millions of Malaria infections occur each year and researching Plasmodium falciparum erythrocyte remodeling may uncover new mitigation efforts. This paper will review research topics covering P. falciparum and the mechanisms used to adapt the erythrocyte to its own needs.