The somatic mutation profile of a tumour may contribute to this; for example, tumours harbouring or acquiring driver mutations in ESR1 [67] or ERBB2 [37] or amplifications at 8p12 (FGFR1) or 11q13 (CCND1) [23] may be less responsive to targeted endocrine therapy. Here, ESR1 is linked to neoplasm.