Another important finding of this work is our observation that the catalytic function of TG2 (transamidation activity) is not essential for NF-κB activation, a finding supported by recent observations suggesting that catalytically inactive mutant forms of TG2 (C277S and W241A) are as effective as the wild-type TG2 in inducing EMT, stem cellness, drug resistance, and an invasive phenotype in cancer cells [24]. Here, NFKB1 is linked to cancer.