Classically, CRC has served as a model for understanding the cooperation of oncogenic mutations (e.g., KRAS, BRAF, PIK3CA, and LIN28B) and the inactivation of tumor suppressor genes (e.g., APC, TP53, and SMAD4) in fostering primary tumorigenesis (3). This evidence concerns the gene PIK3CA and colorectal carcinoma.