In addition to the role in initiation of several tumor types, chronic infection is believed to contribute to cancer progression by activating tumor-promoting signaling pathways (e.g., NF-kB, STAT3), thereby augmenting production of anti-apoptotic proteins, growth factors, and cytokines that foster cancer growth, dissemination and resistance to therapy [1–6]. The gene discussed is STAT3; the disease is neoplasm.