In other words, in gout there is no rift nor lack of finish in the orderly sequence of enzymatic reactions that eventuate in _uric acid_. Uric acid is formed and, as far as we know, after a normal fashion. But, here comes the flaw, viz., the uric acid, when formed, fails of transport and elimination. It is _precipitated_ and _anchored_ in the _tissues_, from whose grip it fails to detach itself. In short, it is not the formation of uric acid, or its failure of further metamorphosis, but the _retention_ of uric acid, and more pertinently, its _fixation in the tissues_ that constitutes the salient feature of gout. Now, all modern research tends to indicate that uric acid is not an intermediary, but a _terminal_ product of metabolism, and, moreover, that there are no _uricolytic_ ferments within the body whereby its destruction can be accomplished. If we grant that— (1) Uric acid is not an intermediate but an end-product of metabolism; and (2) That the human body is devoid of uric acid-destroying enzymes, then it follows that man, _ipso facto_, is _potentially liable to uric acid retention and deposition_, the same objectivated as _tophi_. In this innate potentiality of and to _uratosis_ resides the “gouty” diathesis. If the postulates (1) and (2) be established, then, though it sound rank heresy, it follows that gout is not, chemically speaking, an “error of metabolism.” Not, at any rate, in the ordinary acceptation, viz., not a failure in the transmutation of uric acid into urea and intermediate products. If uric acid be an _end-product_, then no further cleavage into _urea_, etc., occurs, and in this connection the failure to discover _uricolytic enzymes_ is significant. We have before proffered the suggestion that not only local, but _constitutional_, or systemic influences also play a part in the origin of tophi. Provisionally, therefore, we would infer that— (1) The tissues of gouty subjects display an abnormal affinity for uric acid, _i.e._, an increased retention capacity for the same; (2) That certain chemico-physical factors, previously alluded to (content of sodium ions, etc.), favour the incidence of uratic deposits in particular tissues. In other words, we have in these two elements haply the constitutional and local factors that we postulate as essential to the formation of tophi. Albeit, they represent but _latent tissue potentialities_, inadequate of themselves to determine the eruption of _tophi_. Moreover, be it recalled that the _causa causans_ of gout must be responsible not only for the incidence of _tophi_, but also for the more dramatic features of gout, its _arthritic_ outbreaks, etc. To dissociate the cause or causes of the uratic deposits from that of the joint inflammations would indeed appear impermissible.