Several evidence support the involvement of FBXW7 mutations—alongside TP53 and alterations in RTK–RAS signaling pathways—in the progression from normal colonic epithelium to adenoma and carcinoma, suggesting its potential as an early marker of colorectal carcinogenesis and tumor progression through subclonal dysregulation of tumor suppression and DNA repair pathways [82,83]. Here, FBXW7 is linked to neoplasm.