Plasmodium falciparum , the single celled, obligate intracellular parasite responsible for the deadliest form of malaria, has a comparatively compact eukaryotic genome that lacks homologous genes for many regulators of gene expression. Nonetheless, its complex lifecycle circulating from mosquito to human hosts is punctuated by transcriptional bursts and precisely timed translational activity. Methylation of adenosines to N6-methyl-adenosine within mRNA has a diverse range of functional effects, modifying transcript stability and half-life, suppressing translation and altering its efficiency. The mRNA transcripts are methylated at conserved DRACH motifs (D=A,G,T / R = A,G / H = A,C,T). Although the DRACH motif seems to be generally necessary for modification, with most m6A modifications found at DRACH sites, it appears to be insufficient: most DRACH sites are not modified. The reason why only some DRACH sites are modified is poorly understood. We aim to discern the sequence and secondary structural motifs that cause mRNA to be modified with m6A. A mix of existing and novel statistical methods, machine learning approaches and digital encodings of genomic information will be applied to find these motifs. A data pipeline will be built that will allow this analysis to be applied to other species to see if the learnings in Plasmodium falciparum are transferable to other species. Determining the causes of m6a deposition potentially allows engineered biologics to take advantage of the diverse effects of mRNA modification and may offer druggable targets within the parasites themselves that could be exploited by new malaria treatments.