Our results show that tumor suppressive and metabolic effects of a type II tumor suppressor (the carboxypeptidase inhibitor RARRES1 in this case) can be mediated by inhibition of CCP-catalyzed tubulin C-terminal deglutamylation, which in turn directly regulates VDAC1 activity, mitochondrial membrane potential (MMP), reprograms intermediary metabolism and influences cell survival (Figure 6D). The gene discussed is VDAC1; the disease is neoplasm.