Oral carcinogenesis involves early NF-κB activation,289 with TLR2 dyslocalization (entire epithelial layers vs. basal layer-restricted) distinguishing hyperorthokeratosis or dysplasia from normal mucosa in proliferative verrucous leukoplakia.290 TLR4-driven COX-2 induction in Barrett’s esophagus exemplifies microbial pattern recognition receptor (PRR) synergy with inflammation-induced malignant transformation.291 The NF-κB pathway is also closely associated with the pathogen response. Here, NFKB1 is linked to Barrett esophagus.