BCL2 and neoplasm: 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.