In these diseases, CBL, functionally and genetically, acts like a tumour suppressor.8 This hypothesis is supported by a number of studies demonstrating spontaneous activation of RTK signalling pathways in cells with CBL mutations and also limited studies where multitargeted tyrosine kinase inhibitors (TKI's) such as midostaurin or SU112482, 8, 9, 11 can reverse factor independence or factor‐hyperresponsiveness of leukaemia cells.12 This evidence concerns the gene CBL and leukemia.