Notably, aggregating the data for mutant versus wild-type TP53 across all subtypes often led to different results in terms of statistical significance and/or the direction of the effect due to the higher prevalence of TP53 somatic mutations in the basal and Her2-enriched subtypes coupled with differences in gene set expression between the subtypes, emphasising the importance of including tumour subtype as a covariate. The gene discussed is ERBB2; the disease is neoplasm.