Artemisinins are a key component of the combination therapy used to treat malaria. Plasmodium falciparum, the causative agent of the most deadly from of malaria is evolving resistance to artemisinins. The decreased effectiveness of artemisinins increases the probability of resistance to the partner drugs as well; risking total treatment failure which would result in thousands more deaths a year. The gene shown to have the largest affect in modulating resistance is K13. Here we present an RNA-seq study on an isogenic mutant with a dysregulated K13 gene that provides evidence that K13 is involved in regulating DNA replication and repair.