We speculate that FAM168A may act as a linker protein that binds to both BCR-ABL1 and AKT1, and thus participate in BCR-ABL1 protein-mediated sustained phosphorylation of AKT1 protein in CML (Fig. 9). The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.