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Evidence collected over the last 5-7 years indicates that multiple oncogenic mechanisms intercept vesicular transport by introducing mutated or otherwise altered components of vesicular transport mechanisms. Alternatively, evasion of endocytosis and/or enhanced recycling characterize trafficking of oncogenic receptors for growth factors. Finally, several recent studies have raised the intriguing possibility that drug-mediated normalization of vesicular transport may serve as a therapeutic goal in cancer.Cancer cells exhibit altered cellular responses to signals that regulate normal cell survival, proliferation, migration, and differentiation. Pathways that utilize tyrosine phosphorylation as a regulatory mechanism are important in the control of all of these processes.