Gowlland Hopkins, discussing the metabolism of purins, holds that in gout there is some disturbance or defect in the _fermentative functions of the tissues_. Of a verity the range of _intranuclear_ activities offers scope enough when we recollect that the cells of all tissues contain not only _nucleinase_, but also _nucleotidase_ and _nucleosidase_. Even so, the resultant nucleins, the nucleotides, and nucleosides, have still further changes of deaminisation and oxidation to undergo, these carried out in the liver and elsewhere! We may talk of defects in the enzymatic functions of the tissues, but, viewing gout clinically, and more particularly the hypersensitiveness of its victims to the most varied stimuli, dietetic and other, one inclines rather to predicate in their instance an inherent _instability_ of _nuclein metabolism_. For in the gouty, as Walker Hall observes, “a slight injury or indiscretion of diet, an overloaded intestine, or increased toxicity of the intestinal flora, may be followed by a disturbance of the general nuclein metabolism, and a local reaction in certain tissues.” With this pronouncement all clinicians will be in accord, and herein, too, we may, I think, discern how the latent tissue idiosyncrasies of the gouty are evoked, _i.e._, by _infection_; in other words, that, under the influence of these morbific agents, the innate morbid potentialities of the gouty become overt and manifest. The exact _modus operandi_ whereby the assumed organisms or their toxins determine the _efflorescence_ of gout is uncertain. We know that, following the intake even of _non-purin-containing foodstuffs_, an _increase in uric acid excretion_ ensues, and that the same is the outcome of the stimulation of _general_ nuclein metabolism. Is it not conceivable that the responsible toxin acts in like fashion, and haply by disturbing the orderly sequence of those exquisitely delicate enzymatic reactions which culminate in the formation of uric acid, and with which potentialities every living cell in the organism is dowered? Further than this we, pending future researches by the bio-chemists, may not go, for “the positive material is much too insufficient, and much too ambiguous.” In conclusion, I would postulate that in _gouty_ subjects:— (1) There is an inherent abnormality or instability of _nuclein_ metabolism, and conjoined therewith an enhanced tissue affinity or augmented retention capacity for uric acid. (2) These latent tissue peculiarities, through the agency of _infections_ or sub-infections, become manifest as gout. (3) The said organism or organisms excite inflammatory reaction with sequential uratic deposition, either of articular or ab-articular site. (4) The predilection of such uratic deposition for certain particular tissues is determined by their greater content of sodium ions as compared with the blood.