In addition, Fujito et al. demonstrated that ClC-3 and ANO1, by regulating intracellular chloride level, could control the transcription of HER2 in breast cancer cells through the PI3K/Akt/mTOR or STAT3 pathways, depending on the cell/channel type promoting the resistance to anti-HER2 therapies [169]. The gene discussed is ERBB2; the disease is breast carcinoma.