AKT1 and fibrosarcoma: Activating mutations in KRAS usually occur after APC mutations, and its oncogenic mechanism may be highly related to the sustained activation of rapidly accelerated fibrosarcoma (Raf)–mitogen‐activated protein–extracellular signal‐regulated kinase, phosphoinositide 3‐kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) [14].