In the past years, we and others observed that the established length-polymorphic markers, i.e. genes for merozoite surface protein 1 and 2 (msp1, msp2) and glutamate-rich protein (glurp), likely are suboptimal, as major size differences between amplicons cause a bias in amplification efficiency, which in multi-clonal infections leads to preferred amplification of shorter fragments and loss of long alleles2–10. Here, ATAD1 is linked to infection.