In contrast to intracellular MIF, extracellular MIF/CD74 interaction is shown to functionally activate c-Jun phosphorylation and increase AP-1-dependent transcription (35–37) so it is conceivable, if not likely, that the relative balance between extracellular and intracellular MIF levels in a tumor microenvironment or the circulation at any given time dictates the ensuing MIF-associated phenotype. Here, JUN is linked to neoplasm.