As a novel “mutator” mechanism, unscheduled proteolysis of intracellular targets by an “overactive separase” may join the list of so far known tumor escape strategies such as upregulated PI3/AKT pathway, AKT-mediated phosphorylation of FOXO transcription factors, altered Hedgehog and Wnt pathways, and constitutive activation of JAK/STAT signaling [11]. The gene discussed is AKT1; the disease is neoplasm.