A number of studies have shown that the AIS can move over hours or days, with various manipulations such as depolarizing the neuron (as in this study) or stimulating it optogenetically. Two open questions: what are the molecular mechanisms involved in this displacement? Is it actually a displacement or is it just that stuff is removed at one end and inserted at the other end? The same lab previously addressed the first question, showing the involvement of somatic L-type calcium channels and calcineurin. This study shows that myosin (the stuff of muscle, except not the type expressed in muscles) is involved, which strongly suggests that it is an actual displacement; this is in line with previous studies showing that dendrites and axons are contractile structures (e.g. Roland et al. (2014)). This and previous studies start to provide building blocks for a model of activity-dependent structural plasticity of the AIS (working on it!).