Several efforts agree to distinguish four TNBC groups at the level of genes: basal-like immune activated (BLIA) with TP53 mutation and a homologous recombination DNA repair deficiency (HRD) [13]; basal-like immune suppressed (BLIS), which is like BLIA, except for those with a few tumor-infiltrating lymphocytes [14]; mesenchymal-like (MES) with a low mutational burden and PIK3CA mutation [1]; and luminal androgen receptor (LAR), which is characterized by the oncogenic activation of the ER pathway [15]. This evidence concerns the gene TP53 and neoplasm.