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The molecular mechanism by which the PfK13 mutations confer artemisinin resistance in clinical isolates may involve multiple cellular and metabolic processes, including hemoglobin uptake and digestion, the unfolded protein stress response, mitochondrial functions, oxidative stress responses (including tRNA thiouridine modification reprogramming), and an enhanced DNA damage repair mechanism 3, 811, 1320

Oncoimmunology 10 , 1943253 (2021)

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In conclusion, several perspectives on its potential are presented, including new approaches to alterations, directed modification through the association between framework and operation, and the path towards growth for activities and implementations