Insulin causes phosphorylation and inactivation of the Ral GTPase activating complex RGC, causing RalA:GTP to accumulate and associate with the unconventional myosin Myo1c (Chen et al. 2007, Chen et al. 2011). Myo1c motors across cortical actin and interacts with the exocyst complex to tether vesicles at the plasma membrane (Chen et al. 2007).