While others have shown that persistent expression of Myc or Ras oncogenes is required for tumor maintenance [9], K. Podsypanina (Varmus lab) demonstrated that in mammary tumors resulting from coexpression of activated K-Ras with either Myc or Wnt-1, deinduction of K-Ras (using tetracycline regulation) leads to rapid tumor regression. The gene discussed is MYC; the disease is neoplasm.