Targeting signal pathways that were mutated or over-activated during the onset and progression of T-ALL became a new therapeutic strategy, currently included Ras/Raf/MEK/ERK, PI3K/AKT/mTOR, IL-7/JAK/STAT5, and Notch1 signaling pathways [33–39] Activation of ERK was almost present in all T-ALL samples, and activation of MEK/ERK was an independent negative prognostic indicator for T-ALL patients [33, 37]. The gene discussed is AKT1; the disease is acute lymphoblastic leukemia.