As KLF2, an important transcription factor, is mutated in the immune-suppressive NNK SMZL subgroup, future studies might focus on how deregulation of KLF2 or downstream targets results in immune cell reprogramming, recruitment, or evasion, as has been shown for CREBBP and EZH2 in other B-cell lymphomas [82]. This evidence concerns the gene KLF2 and B-cell non-Hodgkin lymphoma.