Consumption of improperly ripened ackee ( Blighia sapida K.D. Koenig) often results in fatalities. The causal toxin, hypoglycin A, decreases in the edible arilli upon maturity; regulation of hypoglycin A in the arilli is thus critical. Hypoglycin B, also toxic, is confined to the seeds. Hypoglycins A and B were tracked in ackees grown in Jamaica over different maturity stages using RP-HPLC. Studies on the 'Butter' and 'Cheese' ackee varieties and across two different harvest seasons were conducted. In 'Cheese' ackees, hypoglycin A decreased from about 8000 mg/kg in the green arilli and seeds to 271 and 1451 mg/kg, respectively, in the ripe fruit whereas hypoglycin B levels in the seeds increased from 1629 to 11774 mg/kg. The strong inverse relationship demonstrated that hypoglycin B in the seeds serves as a sink for hypoglycin A from the ripening arilli and is thereby involved in the detoxification mechanism of the fruit.