Although the antagonizing effect of DIC observed in vivo seems less strong than that observed in the in vitro studies, such a relatively weaker effect can support the NQO1 dependency of TSA in inhibiting the tumor growth, considering that DIC itself can partially retard the tumor growth and that DIC treatment increased the TSA accumulation levels in tumor tissues by inhibiting its metabolic eliminations (Fig. 8) [31]. This evidence concerns the gene NQO1 and neoplasm.