To clarify the mechanisms involved in the repression of BRCA1, and consequently in the impaired FANCD2 foci formation of CML cells, we were interested in further investigating the post-translational regulation of BRCA1 by the proteasome and the PI3K/AKT pathway, frequently activated in human cancer cells, including CML cells[46]. This evidence concerns the gene AKT1 and chronic myelogenous leukemia, BCR-ABL1 positive.