In addition to deregulated BCL2 overexpression, recent studies have revealed the presence of various additional mutations associated with epigenetics (CREBBP, EZH2 KMT2D, MEF2B, ARID1A, etc.), JAK/STAT signalling (SOCS1, STAT6, etc.), BCR/NF-κB signalling (CARD11, TNFAIP3, etc.), and the immune response (TNFRSF14) in FL tumours at diagnosis and were suggested to be involved in both development and disease progression10–12. This evidence concerns the gene CREBBP and neoplasm.