Upon activating TNFR1 on the tumor cells, a phosphorylation of IκB-α on Ser32 and 36 was verified in our study, and such phosphorylation leads to IκB-α degradation, which allows the p50/p65 dimer to enter the nucleus and activate Snail and Zeb2 expression to represse the E-cadherin promoter [42]. The gene discussed is SNAI1; the disease is neoplasm.