Specifically, pancreatic cancer cells with p53 gain-of-function mutations are known for their enhanced migratory capacity, compared to p53 null genotypes, by promoting recycling through endocytic pathways of integrins and EGFR1, dependent on the presence of the Rab11 effector, Rab-coupling protein (RCP) [69]. The gene discussed is RAB11FIP1; the disease is pancreatic neoplasm.