The high frequency of mutations in tumor protein 53 (TP53) dysregulates cell-cycle checkpoints and suppresses apoptosis [9], whereas dysregulation of PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) activates the PI3K/Akt pathway, leading to therapeutic resistance and tumor progression [10]. Here, PIK3CA is linked to neoplasm.