ESR1 and neoplasm: Enrichment of mutations in TP53, GATA3, KMT2C, AKT1, NF1, PTEN, ERBB2, FGFR4, or amplification of 7p11.2 (EGFR), 8q24 (MYC), 11q13.3 (CCND1) and 20q13.2 (AURKA) may also underpin endocrine therapy resistance as they are more frequently identified in ER+/HER2− breast cancer metastases compared to ER+/HER2− primary tumours; many of these gene mutations are mutually exclusive to ESR1 mutations, emphasising their potential equivalence in driving resistance [78,79,80,95].