Studies of the mechanism of drug resistance in breast cancer have mainly focused on alterations in the expression and signalling of the oestrogen receptor (ER), activation of growth factor receptor (GFR) pathways, cross‐stalk between ER and GFR networks, activation of the PI3K/AKT/mTOR pathway (including PTEN inactivation), activation of NF‐κB signalling and expansion of breast cancer stem cells (BCSCs).3, 4, 5, 6. The gene discussed is PTEN; the disease is breast carcinoma.