ACADVL variants result in long-chain acyl-CoA dehydrogenase deficiency in mitochondria [49], while recent research indicates that tumour-specific T cells can be metabolically reprogrammed via the forced expression of ACADVL, which promoted the survival of tumour-specific T cells in a pancreatic cancer mouse model and improve their immunotherapeutic effects [50]. Here, ACADL is linked to neoplasm.