ALDH1L1 and neoplasm: Furthermore, NADH (reduced nicotinamide adenine dinucleotide) in tumor cells can be converted to ATP as an alternative energy source to support tumor growth.[62] Therefore, when glycolysis is inhibited, tumor cells compensate by increasing ATP synthesis via the mitochondrial pathway to meet physiological demands.[63] Zhao et al.[64] combined the PKM2 inhibitor, zeocitrin (SHK), with the aldehyde dehydrogenase 1 family member L1 (ALDH1L1) inhibitor disulfiram (DSF) and developed a hybrid albumin/lactoferrin nanosystem with BBB‐penetrating abilities (BSA/LF NP).