Collectively, these results demonstrate that every P2 animal injected with the lenti-hPDGF-A-Cre virus developed hPDGFRα-positive lesions, and that hPDGF-A expression and hPDGFRα activity in the context of p53 nullizygocity is necessary to initiate tumorigenesis and to sustain growth since half of tumor-bearing animals that failed to maintain PDGF-A expression did not develop lethal tumors. The gene discussed is TP53; the disease is neoplasm.