G9a methyltransferase activity was further reported to (i) collaborate with the transcription factor YY1 and HDAC1 to disrupt cellular iron homeostasis by repressing ferroxidase hephaestin, resulting in iron accumulation and breast cancer progression [109], (ii) induce breast cancer cell autophagy by modulating the AMPK-mTOR pathways [132], and (iii) promote breast cancer recurrence through the suppression of pro-inflammatory genes [133]. The gene discussed is HEPH; the disease is breast carcinoma.