Translated into the clinical setting, in vitro studies provided several evidences on the role of WNT pathway inhibitors: Hu and colleagues used three drugs (IM, LY294002, and AKTi IV) to inhibit the BCR-ABL1/PI3K/AKT pathway in K562 cells, showing that the inhibition of these kinases induced a decrease of the β-catenin protein (but not the mRNA) and suppressed proliferation of CML progenitors (31). The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.