First and second‐generation proteasome inhibitors (bortezomib, carfilzomib and ixazomib) inhibited the clonogenic potential of the mononuclear cell fraction from BC CML patients (n = 4) at subnanomolar concentrations, with the extent of antiblastic activity clearly anticorrelated with SETD2 expression and H3K36me3 levels: patients with lower SETD2 expression showed lower EC50 when compared with patients with higher SETD2 expression and H3K36me3 levels (Figure 8D). The gene discussed is SETD2; the disease is breast cancer.