RNAi therapeutics targeting TGFB2, including S-ODN, may disrupt the TGFB2-linked signaling networks that promote the proliferation and survival of TGFB2high DIPG cells, lift TGFB2-induced suppression of anti-DIPG immunity, as well as block the Treg-mediated tumor tolerance [40]. This evidence concerns the gene TGFB2 and neoplasm.