Its pathogenesis is a multi-factor and multi-step process, involving infection by microorganisms such as Helicobacter pylori, the activation of proto oncogenes such as FOSL1 (encoding Fos-related antigen 1, also known as Fra-1), BRD4 (encoding bromodomain containing 4), and THY1 (encoding Thy-1 cell surface antigen, also known as CD90), and the inactivation of tumor suppressor genes [6–12]. The gene discussed is BRD4; the disease is infection.