Other possible explanations for the lower strength of associations in basal-like and Her2-enriched subtypes are that basal-like tumours are known to have high levels of intra-tumoural heterogeneity, thus diluting the transcriptional effects of sub-clonal TP53 mutations, while Her2-enriched tumours are primarily driven by ERBB2 copy number amplification events which renders TP53 mutations less important. This evidence concerns the gene TP53 and neoplasm.