Based on the literature, ACBP/DBI can mediate cell-autonomous cancer cell-supportive metabolic effects, as indicated by the fact that glioblastoma growth was enhanced by transfection with the wild-type ACBP/DBI protein but not by a mutant (K32A) that lacks acyl-CoA binding capacity and fails to stimulate fatty acid oxidation,18 but still is able to bind to GABRG2 and to mediate metabolic effects when injected into mice.21 This evidence concerns the gene GABRG2 and glioblastoma.