Thus, beyond the overexpression/amplification of HER2 shared among all of them, each of the molecular subtypes of cHER2+ BC have a different mutational landscape [123-126], e.g., whereas the most frequent genetic alteration expected to be found in luminal A/cHER2+ BC is the mutational activation of PI3K signaling, basal/cHER2+ and claudin-low/cHER2+ BC subtypes almost always contain mutations in TP53 as well as genomic alterations in PTEN (Figure B1-2). The gene discussed is ERBB2; the disease is breast cancer.