Our results demonstrate that RIG-I deficiency in HCC cells induced their stemness, TGF-β1 secretion and tolerogenic TIDCs in the tumor microenvironment and reduced generation of monocyte-derived DCs and the results suggest involvement of CSCs in DC-mediated immune tolerance which enables the development and progression of tumors, increased TGF-β1 being possibly involved at least partly in those events. The gene discussed is RIGI; the disease is neoplasm.