This crosstalk is exemplified by an alcoholic liver disease model in which NF-κB was observed to regulate protein expression levels of the catalytic subunit TERT (158), which in turn modulated NF-κB signaling to promote macrophage polarization toward an inflammatory M1 phenotype with increased expression of IL-6 and TNF-α (162). Here, NFKB1 is linked to alcoholic liver diseases.