Wagner et al. showed that KDM2A is overexpressed in lung tumours, and its upregulation induces promoter demethylation of the dual-specificity phosphatase 3 gene, which leads to constitutive activation of extracellular signal-regulated kinase 1 (ERK1) and ERK2 signalling to promote tumour formation.13 Our previous study showed that KDM2A is increased in breast cancer and is associated with poor patient’s survival.14 Knockdown of KDM2A in breast cancer cells reduced the expression of NOTCH signalling molecules including Jagged1, NOTCH1 and HEY1, and attenuated cancer stemness and angiogenesis. The gene discussed is HEY1; the disease is breast carcinoma.