To preserve proteome homeostasis and survive at higher-than-optimal temperatures, organisms have evolved the conserved heat shock (HS) response (HSR), characterised by increased expression of specific chaperone-encoding genes. In the human blood, malaria parasites are frequently exposed to elevated temperatures associated with host fever episodes. The protective HSR of Plasmodium falciparum, the parasite that produces the vast majority of malaria clinical cases and deaths, is regulated by the tr