Members of this class of receptors, such as Toll-like receptors (TLRs), are on one hand needed to maintain homeostasis between microbiota and epithelium [9,10] but can on the other hand also have detrimental effects: activation of TLRs by microbial effectors triggers inflammatory signaling pathways such as nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells (NF-κB), signal transducer and activator of transcription 3 (STAT3) or nuclear factor of activated T-cells (NFAT), which fuel proliferation, inhibit apoptosis and thus enhance tumor growth [11,12,13,14,15]. The gene discussed is STAT3; the disease is neoplasm.