Malaria is one of the deadliest infectious diseases globally, responsible for over 200 million infections each year. Plasmodium falciparum causes the most severe form of the disease and the most deaths. P. falciparum has a complex life cycle between human and mosquito hosts: the intraerythrocytic asexual cycle is responsible for the symptomatic infection in humans. However, for transmission from human to mosquito, a portion of the parasites gradually differentiate into mature gametocytes, which can be taken up by Anopheles mosquitoes. Current frontline treatment against malaria relies largely on artemisinin combination therapies. Emergence of resistance against artemisinin therefore threatens global malaria control. Resistance maps to mutations in the parasites’ k13 gene coding for the Kelch 13 (K13) protein. During the intraerythrocytic cycle, K13 stabilises the parasites’ cytostome, a double membrane invagination responsible for haemoglobin uptake from the host red blood cell, by forming a ring around the cytostomal neck. Activation of artemisinin requires reaction with haem released from digested haemoglobin. The K13 mutation is thought to cause drug resistance through decreasing cytostomal uptake of haemoglobin. However, how K13 modulates this process is undetermined. K13’s role in gametocyte stages is unknown, and the role of K13 and K13 mutations on parasite transmission is also unresolved. Using an endogenously tagged version of K13, we imaged K13 throughout gametocyte development, using standard fixes as well as ultrastructure expansion microscopy. In early gametocytes, K13 was also resolved to form a ring structure, similar to its asexual counterpart. However, in late-stage gametocytes, which are nearing maturity for mosquito transmission, K13 formed a hollow tubular structure, likely serving a function distinct from nutrient uptake. We will investigate the essentiality of K13 in gametocyte and mosquito stages and investigate its potential role in differential transmission of artemisinin-resistant parasites.