To recapitulate the tumorigenic phenotype shown in the mouse model in which negative feedback on YAP/TAZ is ablated, we characterized tumor-associated cellular phenotypes in the AML-12 normal mouse liver cell line after depletion of SAV1, LATS1, and/or LATS2 proteins with shRNA constructs. The gene discussed is YAP1; the disease is acute myeloid leukemia.