Second, despite the multi-institutional cohort included in this study, we currently cannot define whether the mutually exclusive nature of TERT somatic genetic alterations and TP53 mutations in MBCs are derived from epistatic interactions between these genes in the context of MBC or if this mutual exclusivity is solely the result of the different frequencies of alterations affecting these genes in MBCs with distinct types of predominant metaplastic components. The gene discussed is TERT; the disease is maternal uniparental disomy of chromosome 20.