The observed link between molecular subtype and activating mutations in ESR1 (Luminal A/B) and ERBB2/BRAF (HER2-E) hints at the following possibility for the cases where there are both ESR1 and RTK/MAPK oncogenic alterations (e.g., in NF1 and FGFR1): ESR1 mutations drive the tumor towards an ER pathway-dependent transcriptional state that cannot be overcome by RTK/MAPK alterations, resulting in a low RTK pathway signature activity and a Luminal A or B subtype. This evidence concerns the gene ERBB2 and neoplasm.