observed that BRAFV600E downregulates ACACB expression, thereby disrupting the regulation of lipid metabolism, which promotes de-novo lipogenesis and reduces fatty acid oxidation (FAO), synergistically contributing to vemurafenib resistance and increased tumor growth, suggesting that rescuing ACACB may represent a novel strategy to overcome resistance to BRAFV600E inhibitors in PTC and improve treatment outcomes for patients with refractory disease (52). Here, ACACB is linked to neoplasm.