Since 3-OBA is a natural substrate of OXCT1, its availability likely fuels OXCT1-mediated ketone body metabolism, which enhances energetic and biosynthetic capacity in cancer cells, thus promoting tumor progression, moreover, elevated 3-OBA levels could potentiate OXCT1-driven metabolic pathways linked to oncogenic signaling, as OXCT1 activity maintains ketone body homeostasis and activates pro-survival pathways such as NF-κB signaling via complex molecular crosstalk [35]. This evidence concerns the gene NFKB1 and neoplasm.