One of the earliest steps in the development of the neuromuscular junction (NMJ) is the pre-patterning of acetylcholine receptors (AChR) in the center of muscle fibers. This process has recently been proposed to depend on L-type calcium currents. But its feeble current properties make the skeletal muscle calcium channel (Ca(v)1.1) a poor candidate for this function. Independently a new Ca(v)1.1e splice variant with greatly distinct current properties has been described. But so far this channel lacked a function. Could this orphan channel be responsible for regulating AChR pre-patterning? Here we compare the properties of the two splice variants and argue that the newly discovered variant Ca(v)1.1e, is dominantly expressed at the proper time in development and has the essential current properties to accomplish the proposed role in the formation of the NMJ.