Biosynthesis of toxins uses precious cellular energy and it would seem unlikely that evolution would be forgiving enough to tolerate wasted metabolism. Although there is much debate about this proposition in the guise of secondary vs primary metabolites (1,2), it is a reasonable hypothesis that toxins of all kinds should play some beneficial role. This return is apparent when one considers toxins used for prey capture or self-defense as occurs with venoms. For microbial neurotoxins, however, the identity of this biological profit remains a mystery. This is especially so when one considers that the microbes that manufacture these toxins, and those microorganisms that surround them, do not possess nerves nor many of the molecular systems that characterize nerves. The few exceptions to this rule are those microbial toxins that attack generic cellular systems common to many cell types, including nerve cells. An example is the dinoflagellate toxin okadaic acid, an inhibitor of certain serine-threonine protein phosphatases, enzymes that occur widely in different cell types in animals and plants as well as microorganisms (3–5). In fact, an okadaic acid sensitive form of this enzyme has been isolated from the dinoflagellate, Prorocentrum lima, an established producer of okadaic acid (6).One can hypothesize then that okadaic acid may act as a physiological regulator of this enzyme within the dinoflagellate itself or upon unrelated microbes in its vicinity. The larger mystery lies with microbial neurotoxins that attack cellular and molecular neural processes not present in microbes.