Salicylic acid was found capable of uncoupling phosphorylation from the oxidation of β-hydroxybutyrate, glutamate and Fe++-cytochrome c at concentrations in the range of 10−4M. In an acceptor-free system it stimulated oxygen uptake and acetoacetate formation from β-hydroxybutyrate. It is also inhibitory to the phosphorylations accompanying K3Fe(CN)6 reduction with both β-hydroxybutyrate and glutamate; oxidation of the latter substrate appears to be the more susceptible process. Salicylic acid influenced the following processes in a manner consistent with other known uncoupling agents: latent ATPase activity; 32Pi:ATP exchange; and mitochondrial swelling in hypotonic media. The data indicate that the compound is capable of an uncoupling activity qualitatively similar to that of DNP.