HypoExos from tumor cells can enhance oxidative phosphorylation in infiltrating monocytes−macrophages via transfer of let-7a miRNA, resulting in suppression of the insulin-Akt-mTOR signaling pathway [215], and HypoExos (for example, HypoExo circZNF91 from pancreatic cancer cells [216] and HypoExo PKM2 from NSCLC [217]) can promote glycolysis in receptor cells, resulting in treatment resistance. This evidence concerns the gene AKT1 and neoplasm.