In addition, it has been clarified that CHKA positively regulates AKT phosphorylation at the Ser473 residue and is required for the activation of AKT in breast carcinoma cells [55] and that genetic silencing and pharmacological inhibition of CHKA suppresses both PI3K/AKT and MAPK signaling in HeLa cells and T-lymphoma cells [18, 25, 26]. The gene discussed is AKT1; the disease is lymphoma.