Apart from _statistical_ proof of heredity, how else, save on the basis of an _organic predisposition_ to the disease, can we explain the fact that of a large number of individuals, of slothful habit, and given to alcoholic and dietetic excesses, not one may get _gout_; while others who lead literally “a godly, sober, and righteous life,” become martyrs thereto. How escape then the conviction that in gout “breed is stronger than pasture”? for, apart from gluttony and indolence, gout is much more prone to arise in persons in whose pedigree it can be traced than in others. It is not gout, but the _predisposition_ thereto, that is inherited. This proclivity, moreover, may descend to the children of those who, in their own persons, have never suffered from the disease. In Luff’s series it was so in 27 per cent. of the cases, _i.e._, the disease was transmitted from grandparents to grandchildren without the fathers or mothers suffering from “active gout.” In other words, the morbid potentiality may lie _latent_ until _evoked_. Thus, the _females_ of “gouty” families, infinitely more often than not, escape overt gout, but hand on nevertheless their inborn liability thereto to their offspring. Looked at in this light, I see no difficulty in accepting the fact that gout may skip a generation. The son of a gouty parent, happily warned by the excesses of his father, may remain immune, while in turn his son, forgetful of his evil heritage, may bring it again to fruition. The more one reflects on the essential cause of gout, the more inevitable seems the conclusion that gouty individuals, as Walker-Hall contends, “possess some inborn defect or alteration of nuclein metabolism.” And the vague phrases “constitutional” or “nutritional,” as applied by older writers to the disorder, are only explicable on the basis of _inherited structural peculiarities_, with their correlated perversions of tissue function. That such constitute the pathological groundwork of gout, is, I think, further indicated by the fact that _“gouty” inflammation_, in virtue of its associated _uratic deposition_, is _sui generis_. No tissues, other than the _gouty_, react in this _specific_ fashion. Does not this seem to indicate that the _inborn tissue peculiarities_ dictate, so to speak, the _character_ of the pathological reaction; this indifferently, whatever the nature of the so-called _predisposing_ causes which, if our assumption be correct, are merely _provocative_ of gout, in other words, do but evoke or make _manifest_ what is already latent. To sum up, on statistical, and more cogently, general clinical and pathological grounds, my own conclusions are that— (1) Gout is always an hereditary disease. (2) The factors currently regarded as predisposing agencies are in reality merely _determining_ agents, not the cause of gout, but the _occasion of its appearance_.