Genetic mechanisms (mutations, amplifications, fusions) behind the metabolic transformation in tumors that activate PI3K or its effectors, affect genes, such as Her2/neu (e.g., breast cancer), breakpoint cluster region-Abelson murine leukemia viral oncogene homolog (BCR-ABL) (e.g., chronic myeloid leukemia (CML), acute lymphoblastic leukemia (ALL), phosphatase and tensin homolog (PTEN) (e.g., glioma) and Akt2 (e.g., ovarian cancer) [147,149]. This evidence concerns the gene ABL1 and acute lymphoblastic leukemia.