TP53, PIK3CA, and PTEN mutations appear to be acquired early in tumorigenesis, whereas mutations involving cell motility and epithelial-to-mesenchymal transition genes display lower clonal frequencies, suggesting that those represent later events in tumor evolution.17 Importantly, in a substantial fraction of tumors, founder somatic mutations such as TP53 and PIK3CA can be subclonal,17 providing evidence to suggest that a large subset of TNBCs are composed of mosaics of cancer cells at diagnosis.17 The gene discussed is TP53; the disease is cancer.