In this context, gap junction formation was mediated by connexin43 (Cx43) and protocadherin (Pcdh7) and activated the innate immune response pathway cGAS-Sting (Cyclic GMP-AMP synthase-stimulator of interferon genes) leading to secretion of tumor-supportive cytokines such as IFNα and TNF (Figure 1; Box 3). The gene discussed is GJA1; the disease is neoplasm.