Constitutive expression of c-MYC has been discovered in carcinomas of the cervix, colon, breast, stomach, and lung.38 39 Recently, abnormal expression or activation of c-MYC was reported in immune cells, indicating that c-MYC regulates the TME, thereby activating angiogenesis and suppressing the host immune response.40–42 For example, c-MYC inactivation in an immunocompromised RAG1−/− host (deficient for B and T cells) or a CD4−/− host (deficient in CD4+ T-helper cells) reduced the kinetics of tumor regression, increased minimal residual disease, and promoted inevitable tumor recurrence. The gene discussed is MYC; the disease is neoplasm.