Our data that p52SHC-KO rats have increased latency and decreased tumor multiplicity suggest that delayed onset of tumorigenesis observed in the mouse model of polyomavirus middle T antigen (MT)-induced mammary tumors in which critical tyrosine phosphorylation residues in SHCA are mutated (termed ShcA3F and ShcA2F) resulting in fewer tumors are likely due to phosphorylation defects of the p52SHC isoform [17]. The gene discussed is SHC1; the disease is neoplasm.