We previously showed that upregulation of the receptor tyrosine kinase (RTK)s of the epidermal growth factor receptor (EGFR) family was a major cause of PCa recurrence following AR inhibition.8 The EGFR family is comprised of four members: EGFR/ErbB1, HER2/ErbB2, HER3/ErbB3 and HER4/ErbB4 that are activated by ligand-binding (except HER2), followed by dimerisation and phosphorylation.9 HER2 exists in a constitutively ‘open’ conformation and is the preferred dimerisation partner for EGFR and HER2. The gene discussed is ERBB2; the disease is posterior cortical atrophy.