Schematic model indicating the presence of two potential insulin receptor–dependent signal transduction pathways. In this model, insulin stimulation results in the activation of a PI 3-kinase–dependent pathway that is necessary but not sufficient to induce GLUT4 translocation. In parallel, the insulin receptor activates an additional pathway leading to Cbl tyrosine phosphorylation through its interaction with the CAP protein. Syn4, syntaxin 4; PI3-K, PI 3-kinase.