SOAT1 and aneurysmal bone cyst: The main molecular and genetic abnormalities in GCB DLBCL include activation of PI3K/AKT/mTOR pathway, BCL2 translocations, and BCL6 rearrangements and overexpression, MYC rearrangements, and EZH2 mutations; while ABC DLBCL is featured with the activation of BCR, NF-κB and JAK-STAT pathways with associated mutations in genes including CD79A/B, CARD11, TNFAIP3 (A20) and MYD88. For PMBL DLBCL, key molecular abnormalities include CIITA translocations, amplification of REL, amplification of chromosome region 9p24 containing PD-L1, PD-L2 and JAK2 loci, and activation of NF-κB pathways [3, 7, 8].