If this hypothesis is correct, one could predict that co-expression of an anti-apoptotic mediator, such as Mcl-1, would rescue TGFβ1 dependent tumor inhibition phenotype, i.e., overexpression of TGFβ1 would not be able to suppress tumor development induced by c-Myc and Mcl-1 oncogenes in the liver. The gene discussed is MCL1; the disease is neoplasm.