Recent studies have suggested that axis could be a promising target in T ALL, as in over 70 of T ALL patients, PI3K/Akt/mTOR signaling is constitutively activated and portends an undesirable prognosis. In light of this, it is essential to develop new therapeutic strategies against T ALL cells aimed to negatively regulate this sign cascade for improving the clinical outcome Canagliflozin SGLT Inhibitors of the patients. Since aberrant PI3K/Akt/mTOR process activation plays a crucial role in the pathogenesis of T ALL, the goal of this research is to try and compare the healing potential of selective inhibitors, such as for instance GDC 0941, MK 2206, NVP BAG956, RAD 001, and KU 63794. In this study, we examined these drugs either alone or in combination, against T ALL cell lines and primary examples from T ALL patients. The highest cytotoxic potential against T ALL cell lines and patient lymphoblasts was shown by NVP BAG956, a dual PI3K/PDK1 inhibitor that has demonstrated an ability to be Eumycetoma effective against BCR ABL and mutant FLT3 revealing acute leukemia cells. Therefore, NVP BAG956 is documented to affect proliferation of melanoma cells. To our knowledge this may be the first-time this drug is employed against T ALL cells. NVP BAG956 was largely cytostatic in T ALL cell lines and was not a strong inducer of apoptosis. Nevertheless, it potently induced apoptosis in T ALL key cells, including a cell subset that is enriched in putative LICs. GDC 0941 can be an inhibitor of class I PI3K that’s entered clinical trials for solid tumors. In T ALL cell lines and individual samples, GDC 0941 displayed a poor cytostatic effect. MOLT 4 cells were more sensitive and painful to GDC 0941 compared to the other cell lines. The allosteric Akt chemical MK 2206, that is presently undergoing clinical trials for the Aurora Kinase Inhibitors therapy of solid tumors, was more powerful than GDC 0941 in both T ALL cell lines and primary examples. Aside from being cytostatic, MK 2206 also induced apoptosis. Surprisingly, we discovered that RAD 001 was more powerful than KU 63794, an ATP competitive mTORC1/mTORC2 inhibitor, specially in MOLT 4 cells. Indeed, ATP competitive mTORC1/mTORC2 inhibitors are usually regarded as being more powerful than rapamycin and rapalogs. But, KU 63794 and RAD 001 displayed not quite similar fragile potency against T ALL lymphoblasts. A fascinating observation is that RAD 001 treatment led to Ser 473 p Akt dephosphorylation in T ALL cell lines. In many cancer Akt phosphorylation was increased by cell types, rapalogs such as RAD 001, through inhibition of the negative feed back loop depending on mTORC1/p70S6K/IRS1/PI3K. Inhibition of this type of negative feed-back loop up handles mTORC2 dependent phosphorylation of Akt on Ser 473 and increases cell survival. However, the rapalog chemical CCI 779 has been reported to cause mTORC2 dis-assembly and Ser 473 r Akt dephosphorylation.