CK2 is overexpressed in primary T-ALL cells [2,15], and CK2-mediated phosphorylation of phosphatase and tensin homologue (PTEN) at S380 induces the stabilization of the phosphatase in a non-functional state [20], leading to aberrant PI3K/Akt signaling activation and consequently increased leukemia cell survival and proliferation [2]. The gene discussed is AKT1; the disease is acute lymphoblastic leukemia.