Non-genetic adaptive resistance mechanisms to targeted therapies, such as these, are poorly described in DLBCL and have not been characterized for transcription factor targeted therapy, yet are critically important as exemplified in non-small cell lung cancer for anti-EGFR signaling drugs [12] and in B-cell acute lymphoid leukemia for tyrosine kinase inhibitors [8]. Here, EGFR is linked to diffuse large B-cell lymphoma.