They cause atemporary and specific opening of tight junctions that allows varioustherapeutic agents to penetrate tumors[74, 75].It seems possible that the combined use of DNase I and “junction openers”could increase the effectiveness of anticancer therapy, since it wouldfacilitate the effective penetration of agents, including cytotoxic cells, intothe depths of a malignant neoplasm. This evidence concerns the gene DNASE1 and cancer.