AKT1 and neoplasm: Resistance to therapies targeting MYC and mTOR can arise through multiple mechanisms, including compensatory activation of alternative pathways (PI3K/AKT, MAPK/ERK), feedback loops (MYC-mTOR signaling feedback), tumor heterogeneity (clonal evolution), alterations in the tumor microenvironment (metabolic or hypoxic), and drug resistance through ABC Transporters (P-glycoproteins) [134–136].