Our bioinformatic survey revealed that among the downregulated genes, E2F7 acted as a direct suppressor of the transcriptional activity of E2F1, strengthening the hypothesis that an mTORC2-Akt-E2F1 axis might be involved in controlling CML-LSCs properties. This evidence concerns the gene E2F7 and chronic myelogenous leukemia, BCR-ABL1 positive.