PTEN and acute lymphoblastic leukemia: Subpopulations of T-ALL patients and cell lines (including CEM, SUP-T1, and Jurkat cells) are insensitive to GSI therapy, presumably due to mutations that result in constitutive ICN expression or additional mutations in genes downstream [8] such as phosphatase and tensin homolog (PTEN), a tumor suppressor and negative regulator of the PI3K/AKT/mTOR signaling pathway [11].