KRT17 and triple-negative breast carcinoma: Here we for the first time show strong evidence based on integrated clinical and genetic information that, C19MC expression specifically marks TNBCs and that, RESTlow status might drive the expression of KRT5, KRT14, and KRT17 through CEBPB-dependent enhancer activation, and target PGR, ESR1, and ERBB2 mRNAs through C19MC miRNAs to potentially drive triple negative breast cancers (Fig 7A).