Key pathways include cell cycle regulation with overexpressed cyclin-dependent kinases (CDKs), leading to unchecked cell division (21); the PI3K/AKT/mTOR pathway, which is hyperactivated, promoting tumor growth and therapy resistance (22); and DNA repair defects involving BRCA1/2 (23) and PARP (24), making tumors more susceptible to specific treatments. This evidence concerns the gene AKT1 and neoplasm.