We assessed the mutation distribution of the major pathways associated with the pathogenesis of DLBCL which including BCR signaling, NF-kB, mammalian target of rapamycin (mTOR), phosphoinositide 3-kinase (PI3K)-protein kinase B (Akt), and JAK/STAT pathways. This evidence concerns the gene SOAT1 and diffuse large B-cell lymphoma.