Successively, promoted by Kirsten rat sarcoma virus (KRAS) oncogene activation and serine/threonine-protein kinase B-Raf (BRAF) mutations along with chromosomal (microsatellite) instabilities, high-grade dysplasia will develop that accelerate transformation to malignant progression and invasive carcinoma by further accumulating p53 mutations. This evidence concerns the gene BRAF and invasive carcinoma.