Such defects can be overcome by the administration of non-enterotoxin-producing strains of B. fragilis, immunization with immunostimulatory B. fragilis polysaccharide, or by adoptive transfer of B. fragilis-specific T-cells, in which the mechanisms underlie the restoration of therapeutic response to CTLA-4 blockade is suggested to be via induction of the IL-12-dependent TH1 immune response in tumor-draining lymph nodes, and stimulation of intratumoral dendritic cells (DCs) maturation (Vétizou et al., 2015). The gene discussed is CTLA4; the disease is neoplasm.