Palbociclib clinical trial between strains with different pfhrp2 sequence. Control of transcription is believed to be under the influence of various regulatory systems, many of which are incompletely understood in Plasmodia. It is clear that transcription patterns vary between genetically distinct parasites. The 59 untranslated region of genes may contain regulatory elements that interact with promoter region elements to regulate transcription, or influence mRNA stability or survival. The 39 UTR may also have an important role n regulation of gene function. Although not investigated in this study, different parasite lines with different pfhrp2, or even identical coding sequences may differ in their 59 UTR and 39 UTR sequences, resulting in different levels of transcription. Epigenetic mechanisms may also significantly affect transcription. Changes in chromatin structure may profoundly influence the relationship between promoter and transcription factors. Nucleosome-free regions found at transcription start sites and core promoters are strongly associated with high levels of gene expression in intraerythrocytic stages. It is therefore possible that epigenetic factors play a role in pfhrp2 and pfhrp3 transcription. It should be noted that the levels of pfhrp2 and pfhrp3 transcripts and PfHRP protein measured in this study constitute the amounts of transcript or protein present at that timepoint, reflecting the combined result of transcription and degradation of the target. For transcripts, post-transcriptional control mechanisms including mRNA stability and decay may contribute significantly to the variation in the amount of transcripts present. mRNA translation efficiency can also be influenced by a range of factors. Histone 396–494 of pfhrp3 may play a role in mRNA stability. Variation in binding factor sequences in the 59 and 39 UTR may also exert a significant influence on mRNA stability and translation. Likewise, changes to the transcription start site may regulate the translation efficiency of a given gene. In all strains tested in this study, we observed that the level of pfhrp2 transcripts was always higher than that of pfhrp3. This could be a consequence of the promoter for pfhrp2 being stronger, or as a result of a slower decay of pfhrp2 transcripts. A 59 flanking region of pfhrp3 has been extensively used in transfection studies as a promoter for reporter gene expression, paired with a 39 flanking region of pfhrp2 as a terminator sequence. However, there is no report of using the pfhrp2 promoter for transfection, thus precluding a comparison of the two promoters.