Using multi-omics datasets of TNBC, the heterogeneity of tumor microenvironment it was explored, providing evidence about three different clusters: cluster 1 was characterized by an incapability to attract immune cells, and MYC amplification was correlated with a low immune response; cluster 2 was characterized by chemotaxis, but inactivation of innate immunity and low tumor antigen burden, thus contributing to immune escape, in association with mutations of the PI3K-AKT pathway; cluster 3 was characterized by a high expression of immune checkpoint molecules [124]. The gene discussed is AKT1; the disease is neoplasm.