The in vivo study showed that even though neither PIDD nor caspase-2 failed to suppress lymphoma formation triggered by γ-irradiation or 3-methylcholanthrene-driven fibrosarcoma development, caspase-2 was anti-tumorigenic in response to aberrant c-Myc expression (a carcinogen forming bulky adducts with DNA), independently of PIDD, Bid or Trail and caspase-2 mediated tumor suppression was associated with reduced rates of p53 loss and increased dissemination potential of tumor cells. The gene discussed is PIDD1; the disease is neoplasm.