The evidence that IFN-γ+ T cells were not produced, and tumor growth was not inhibited in TLR-2-knock-out mice following administration of HP-NAP (40) or by co-administrating rMBP-NAP and a TLR-2 blocking antibody (41), confirmed the in vitro finding suggesting the essential role of the immune receptor for the HP-NAP activity (18). This evidence concerns the gene CTNNBL1 and neoplasm.