Several mechanisms have been proposed to explain the improved efficacy with cytotoxic agents and include increased diffusion of chemotherapy and payload-containing particles such as liposomes into tumor masses [45], [46], reversal of chemotherapy resistance [29], [41], inhibition of DNA repair by blockade of γH2AX foci formation [28] and reversal of TGFβ-induced accumulation of tumor cells in G0/G1[21], [44]. The gene discussed is TGFB1; the disease is neoplasm.