The upregulation of de novo lipid synthesis (DNL)is cited as abiomarker of aggressive PCa disease,5 whileinhibiting DNL has therapeutic potential for PCa treatment.6 The overexpression of several key enzymes (e.g.,acetyl-coA carboxylase, ACC, and fatty acid synthase, FAS) involvedin DNL (Figure 1A)stimulates energy fluxes to meet metabolic lipid demands.7 One such example is 5-(tetradecyloxy)-2-furoicacid (TOFA) which inhibits the rate-limiting enzyme, ACC responsiblefor the conversion of acetyl-CoA into malonyl-CoA (Figure 1B). The gene discussed is FAS; the disease is posterior cortical atrophy.