NFKB1 and neoplasm: In CRC, intratumoral bacteria sustain the activation of the NFκB-TNF-α-IL-6 pathway to promote the activation of metalloproteins and colony-stimulating factor 1–3 (CSF1-3) to result in an increased risk of relapse [144, 145], and also increase the mortality by reducing tumor-infiltrating lymphocytes infiltration [146].