1. 1. Dark pretreatment of chloroplasts with high concentrations of KCN in the presence of a trace of ferricyanide completely blocks subsequent transfer of electrons from water to hydrophilic acceptors such as ferricyanide and methylviologen. In the KCN-treated chloroplasts there is still a largely uninhibited electron flow from water to lipophilic oxidants such as p-benzoquinonediimide (oxidized p-phenylenediamine), duroquinonediimide (oxidized diaminodurene) and 2,5-dimethyl- p-benzoquinone. The cyanide-insensitive electron transport supports phosphorylation with a P/ e 2 ratio of 0.3 to 0.4. It is concluded (a) that these lipophilic oxidants can accept electrons from an unknown intermediate carrier, X, which precedes the KCN-inhibition site and is inaccessible to hydrophilic oxidants, and (b) that a phosphorylation site is associated with the electron pathway H 2O→X. 2. 2. Electron transport from diaminodurene to methylviologen and the associated phosphorylation are both inhibited by KCN. The same is true of cyclic photophosphorylation reactions catalyzed by diaminodurene, reduced dichlorophenolindophenol, pyocyanine, and low concentrations of N-methylphenazonium methosulfate. However, cyclic photophosphorylation can be largely restored by high concentrations of PMS. 3. 3. Isolated plastocyanin reacts readily with high concentrations of KCN (> 10 mM) but only at the relatively high pH values (> 7.5) required for effective KCN treatment of chloroplasts. It is suggested that this copper protein is the site of KCN inhibition in chloroplasts. 4. 4. Photoreduction of p-benzoquinonediimide is extremely sensitive to Photosystem II inhibitors, such as 3-(3,4-dichlorophenyl)-1,1-dimethylurea, and the inhibition is completely independent of light intensity. In contrast, although the reduction of ferricyanide is almost equally sensitive at very low light intensities, the sensitivity decreases as the light intensity increases. It is suggested that the lipophilic reduction site, X, may be located close to Photosystem II.