The mechanism underlying the hyperammonemia and lactic acidosis induced by 5-FU involves its hepatic metabolism by dihydropyrimidine dehydrogenase, resulting in the formation of alpha-fluoro-beta-alanine and ammonia, which is further metabolized to fluoro-acetate, inhibiting the tricarboxylic acid (TCA) cycle. The gene discussed is DPYD; the disease is lactic acidosis.