Although the characterization of the molecular mechanisms behind this observation are beside the scope of the present paper, we may speculate that MIF/DDT inhibition could improve the activity of p53, inhibiting cell-cycle progression, anchorage independence, and increasing programmed cell death, as previously shown in human lung adenocarcinoma cell lines by [23] and, consequently reducing the IC50 of vincristine. Here, MIF is linked to lung adenocarcinoma.