These studies partially validate our anticipated differential mechanisms and suggest that KRT19 directly interacts with either the β-catenin-RAC1 complex to induce nuclear import of β-catenin/RAC1 and to consequently activate NUMB transcription and promote Notch signaling crosstalk in breast cancer or β-catenin only, leading to β-catenin stability and nuclear translocation, regardless of RAC1, then Wnt/β-catenin/Notch signaling pathway-mediated colon cancer progression. This evidence concerns the gene RAC1 and breast cancer.