There were copy number amplification and copy number loss of PI3K (without PIK3R1) and AKT subunits in DLBCL patients, and the copy number variation of PIK3CA was highly correlated with abnormal p110α protein expression and subsequent PI3K/AKT pathway activation, which was significant for the prognosis of DLBCL patients [13]. The gene discussed is AKT1; the disease is diffuse large B-cell lymphoma.