So, EBV reactivation in an immune-privileged site, as supported by PD-L1 upregulation indicating immune escape, might play a role in the pathogenesis of EBV + BIA-DLBCL, possibly assisted by genetic aberrations as were found in MPS results in lymphoma associated genes DDX3X, EZH2 and NFKBIE of the mass-forming lesion in Case 1 [15, 16]. Here, EZH2 is linked to diffuse large B-cell lymphoma.