Mcl‐1 has a very short half‐life, and its expression is tightly regulated by its interaction with FBW7, which also mediates its degradation.32, 39, 40 FBW7 mutations in tumours have been shown to increase Mcl‐1 expression to augment resistance to both standard chemotherapy and targeted therapy.32, 38, 41, 42 The pathogenesis and poor prognosis arising from elevated Mcl‐1 protein levels in refractory cancers are suggestive of manipulating the protein rather than the mRNA to boost apoptosis and thereby target a malignancy. The gene discussed is MCL1; the disease is cancer.