Targeting PPIs between DNA glycosylases and their cellular partners that are enhanced in tumors, as was done for the NTH1-YB1 interaction [162], constitutes a new and original approach, which has the advantage of not blocking DNA repair in normal, healthy cells, but instead to specifically inhibit the upregulation of DNA repair activity in drug-resistant tumor cells. The gene discussed is NTHL1; the disease is neoplasm.