The first clues to the role of septins in neoplasia came from the observation that balanced translocations involving septin loci and the MLL locus on chromosome 11 were seen in leukaemia giving rise to chimeric fusion proteins where the N terminus of MLL was fused, in frame, to almost the entire open reading frame of SEPT9 (Osaka et al, 1999). This evidence concerns the gene KMT2A and neoplasm.