In laboratory models, treatment with cET-ASO^KRas reduced mutant KRAS levels and inhibited the growth of pancreatic cancer cells and tumor-like spheroids. This allowed cET-ASO^KRas to escape into the cytoplasm, where it could bind to mutant KRAS messenger RNA. The researchers demonstrated the importance of this pathway by removing CD44 or EPHA2 from pancreatic cancer cells. By understanding how cancer cells import, transport, and restrict these drugs, scientists may be able to turn their own trafficking systems into a delivery advantage. Keywords: Antisense oligonucleotides, ASO therapy, KRAS, pancreatic cancer, CD44, EPHA2, endocytosis, endosomal trafficking, endosomal escape, stress granules, ISRIB, cancer treatment, molecular biology