In addition to exploiting the metabolic properties of ACTs themselves to overcome the short lifespan and persistence of adoptively transferred immune cells, pharmacological metabolic interventions aimed at targeting tumor-associated FASN may prime cancer cells for mitochondrial apoptosis, resulting in a more robust and durable response of FASN-dependent tumors to ACPs-mediated cytolysis. This evidence concerns the gene AASDHPPT and neoplasm.