The Turing mechanism for the production of a broken spatial symmetry in an initially homogeneous system of reacting and diffusing substances has attracted much interest as a potential model for certain aspects of morphogenesis such as pre-patterning in the embryo, and has also served as a model for self-organization in more generic systems. The two features necessary for the formation of Turing patterns are short-range autocatalysis and long-range inhibition which usually only occur when the diffusion rate of the inhibitor is significantly greater than that of the activator. This observation has sometimes been used to cast doubt on applicability of the Turing mechanism to cellular patterning since many messenger molecules that diffuse between cells do so at more-or-less similar rates. Here we show that stationary, symmetry-breaking Turing patterns can form in physiologically realistic systems even when the extracellular diffusion coefficients are equal; the kinetic properties of the 'receiver' and 'transmitter' proteins responsible for signal transduction will be primary factors governing this process.