We found that β-oxidation and its regulator CPT1 A/C mRNA levels were both downregulated in NE-like PCa cells, suggesting that NE-like PCa cells are less dependent on the fatty acid uptake and β-oxidation, which is further supported by the observation that CPT1 inhibitor did not have effects on the proliferation of NE-like PCa cells. Here, CPT1A is linked to posterior cortical atrophy.