KRAS and Familial prostate cancer: These results are in line with previous observations in breast tumors, showing that those with a partial EMT state display a higher metastatic capacity than fully dedifferentiated ones [34], and in prostate cancer mouse models showing that KRas overexpression in Pten-null PECs promotes intermediate epithelial-mesenchymal states with high tumoroid-forming capacity and metastasis to soft tissues [35, 36].