The disconnect between assumed AKT signaling dependency and drug potency is further exemplified by the finding that treatment with the pan-AKT inhibitor, MK2206, in a xenograft model of MCF-7 and MDA-MB-231 human breast cancer cells, increased in vivo lung metastasis, whereas AKT1 knockdown inhibited the invasiveness of the two xenografts [264]. The gene discussed is AKT1; the disease is breast cancer.