Resistance to artemisinin and its derivatives is becoming a serious threat to current antimalarial drug therapy. Understanding the molecular mechanisms underlying artemisinin resistance will aid drug development and malaria control. Recently, genetic screens have identified the involvement of the Kelch13 gene in screens of clinical samples with a slow parasite clearance time, and PfMDR1 gene amplification in laboratory-derived strains of P. falciparum resistant to 80 ng/ml artelinic acid, a semi-synthetic derivative of artemisinin. In these resistant strains, the resistance phenotype has been demonstrated to have (i) decreased sensitivity of mature-stage parasites, (ii) decreased sensitivity of the ring stage to the induction of dormancy, and (iii) a faster recovery from dormancy. In an effort to identify proteins and pathways involved in the resistance phenotype, we have used Orbitrap mass spectrometry-based proteomics to compare global protein expression levels in parallel cultures of resistant and wild-type strains. This has identified 11 proteins whose expression is significantly associated with artelinic acid resistance.These proteins and their potential involvement in artemisinin resistance will be discussed.