To the Editor: In their article describing the development of partial resistance of Plasmodium falciparum to artemisinin therapy in Eritrea, Mihreteab and colleagues (Sept. 28 issue)1 conclude that both Pf kelch13-mediated resistance to artemisinin and deletions in hrp2 and hrp3 threaten to compromise regional malaria control and elimination campaigns. In this regard, in 2014, our group described an analysis of Pfkelch13 R622I in northwest Ethiopia in an in vivo efficacy study involving patients who had been treated with a combination of artemether and lumefantrine.2 Subsequently, in 2017, we documented the expansion of R622I (from 2.4 to 9.5%), although all the treated patients had cleared parasites by day 3.3 Our data regarding artemether–lumefantrine therapy contrast with those reported by Mihreteab et al., possibly because of the lower median age of the patients in their study (15 years vs. 19 in our study). In addition, the artificial mutant strains that were created in their study may not reflect the phenotype of actual isolates that are typically cultured from patients for the testing of in vitro susceptibility in clinical practice. These factors may have led to an overestimation of the resistance potential of R622I. Moreover, polymerase-chain-reaction (PCR) assays to evaluate the prevalence of hrp2 deletions cannot detect polyclonal infections (with or without hrp2), partial exon deletions, or low-density infections as seen in asymptomatic patients.4 Droplet digital PCR may better detect the complex genetic background of hrp2 deletions, a subject that warrants further investigation.