TLR3 and breast cancer: Recent research highlights that inhibition of TGFβ and activation of NF-κB-mediated inflammatory signaling are critical for shifting human cells from quiescence to regeneration, thus enabling Wnt/β-catenin-induced cell proliferation.266 CSCs are instrumental in tumor initiation and progression.267 Activation of TLR3, both in vitro and in vivo, promotes the transition of BC cells toward a CSC phenotype.267,268 Notably, TLR3 does not rely solely on the conventional NF-κB pathway to enrich CSCs; both the β-catenin and NF-κB pathways are activated in tandem.