The introduction of exogenous Wnt1 partially counteracted the negative impacts of LMP2 and TAP2 overexpression, while the inhibition of endogenous Wnt1 attenuated the tumor-promoting effects of LMP2 and TAP2 depletion, highlighting the pivotal role of the Wnt1 pathway in mediating the biological functions of LMP2 and TAP2 in cervical cancer cells. The gene discussed is WNT1; the disease is neoplasm.