Together, these depletion, overexpression, and ChIP experiments indicate that STAT3, MYC, and EBNA1 are not only critical for cell survival and proliferation in EBV-transformed/cancer cells, but also work in concert to regulate ZC3H18 expression and each other, positioning ZC3H18 as an effector in EBV-driven oncogenesis. The gene discussed is ZC3H18; the disease is cancer.