Several studies suggest that the disorganization of membrane microdomains containing the subpopulations of NaV1.5 channels could also contribute to the substrate of acquired cardiac arrhythmias, for instance, the direct targeting of hemi-channels to the ID via the microtubule plus-end-tracking protein EB1 [90] and the targeting of CaV1.2 to t-tubules by BIN1 (bridging integrator 1), a protein involved in membrane invagination and endocytotic processes [91]. The gene discussed is BIN1; the disease is cardiac rhythm disease.