Malaria affects close to half of the world’s population and kills nearly 3,000 children every day. Due to the rapid rise in drug-resistant parasites and insecticide-resistant mosquitoes, we need a vaccine now more than ever before. Malaria is caused when a mosquito infected with the parasite, Plasmodium, bites and injects thousands of sporozoites that infect the liver and replicate without causing symptoms for 7-10 days. After egressing out of the liver, the parasites infect red blood cells and can get taken up by another mosquito during a bite perpetuating disease transmission. In the blood stage, the population of parasites in circulation can reach the billions, symptoms occur, and disease complications can result in death. Our strategy is to develop a pre-erythrocytic malaria vaccine by creating a genetically attenuated parasite (GAP) strain. If infection could be stopped before the parasites break through into the proliferative blood stage, both the disease and transmission could be prevented. Our goal is to make a late-liver stage arresting Plasmodium falciparum GAP conferring a broad antigenic diversity. Based on late-liver stage transcriptomics, we identified genes that could be candidates for knockout. One of these genes is mei2 of which my team already generated a CRISPR/Cas9-mediated knockout. We conducted an analysis of invasion kinetics via a growth competition assay between wild-type and mei2- parasites to ensure the gene deletion did not reduce viability. We proceeded by exposing our human-liver chimeric mice to infectious mei2- sporozoites, tracked liver stage development, and looked for breakthrough into the blood stage as an indication of incomplete attenuation. We then built on the previously established role of mei2 as an RNA binding protein by studying the subcellular localization of Pf mei2 to better understand the effect it has on liver-stage development.