TLR1 and neoplasm: We speculate that sensitivity to TLR1/2 ligands may lead to enhanced intratumor and/or systemic inflammation triggered by endogenous TLR1/2 ligands [e.g., the gut microbiome (29), tumor microbiome (34, 35), and/or endogenous “self” ligands within the tumor (32, 33)] that could conceivably induce chemokine secretion within the tumor to enable trafficking of antitumor T cells to the tumor site, enhance antitumor T/B-cell functionality, and/or activate tumor local antigen presenting cells.