Malaria is a leading cause of illness and death globally, with nearly half of the world's population being at risk of contracting the disease. Despite this, little is known about the underlying molecular mechanisms behind malaria progression and how this looks like in different populations. This is particularly true of Southeast Asian populations, where multiple adaptations to malaria have been identified, such as Southeast Asian ovalocytosis and G6PD deficiency. This study utilises transcriptomic data from individuals within Indonesia, a country where nearly half of the population lives in malaria-endemic areas. Using transcriptomic data from whole blood of 78 Indonesian samples infected with malaria and 138 healthy controls, I analyse which genes and pathways are involved in plasmodium infection. I find hundreds of genes differentially expressed in sick versus healthy controls, many of which are involved in inflammation, such as S100A8, a gene previously documented in mice and humans infected with malaria. Furthermore, I find an upregulation of many immediate early response genes such as FOS and CD69, as well as genes involved in apoptosis, recognition receptors, and antigen processing.