KRAS is a frequently mutated oncogene that regulates cell division and promotes pancreatic cancer development. Mutations in KRAS increase resistance to chemotherapy and drive cancer cell transformation. Macropinocytosis, an endocytic process, is heightened in KRAS-mutant cancer cells, allowing them to acquire nutrients to meet high metabolic demands. This process can be exploited for targeted drug delivery, including chemotherapeutic agents. The study investigates the uptake of cyclodextrin-based drug carriers in KRAS-mutant pancreatic cancer cells and tests the impact of KRAS inhibitors on macropinocytosis, providing insights into new therapeutic strategies.