Resistance to antimalarials is a recurring hurdle towards effective management and/or elimination of malaria. Decreased susceptibility to artemisinin, the most effective antimalarial currently available, has emerged and its global spread is a serious risk to malaria control. Mutations in the P. falciparum Kelch 13 (PfK13) protein lead to decreased susceptibility to artemisinin. The function of this protein is unknown, but recent evidence shows involvement in the parasite's haemoglobin uptake process. Digestion of haemoglobin taken up by the parasite produces free haem, which is necessary to activate artemisinin and initiates the events leading to parasite death. Using indirect immunofluorescence visualised by super-resolution microscopy, we show that PfK13 forms doughnut-shaped structures located at the parasite periphery. This indicates that PfK13 is located at the parasite's primary uptake structure called the cytostome. Furthermore, fluorescent live cell imaging of GFP-tagged PfK13 (GFP-PfK13) parasite line grown in fluorescent dextran-loaded red blood cells (RBC) show that GFP-PfK13 is closely associated with fluorescent dextran-loaded structures that form inside the parasite as it feeds from the RBC host. In mid-ring stage parasites, fluorescent dextran-loaded structures are also found associated with hemozoin pigments that form prior to the formation of the digestive vacuole. GFP-PfK13 is also seen associated with these structures, indicating involvement of PfK13 in haemoglobin digestion and hemozoin formation. As previously shown, in late ring or trophozoite parasite stage the hemozoin pigments coalesce to form a single digestive vacuole that is fed by haemoglobin-containing vesicles. We show that GFP-PfK13 is associated with such structures, indicating PfK13’s involvement in digestive vacuole biogenesis. Taken together, our results show that PfK13 is closely associated with the haemoglobin uptake process and digestive vacuole biogenesis. Mutations in PfK13 have been shown to lead to a decreased abundance of haemoglobin peptides in the parasite, which can lead to decreased activation of artemisinin and, ultimately, decreased parasite susceptibility.