Altogether, the results presented thus far support the idea that the absence of dystrophin in the DMD iPSC-CMs resulted in reduced abundance of NaV1.5 protein in the whole cell and likely reduced trafficking of both NaV1.5 and Kir2.1 to the cell membrane, as predicted from our previous work (Matamoros et al., 2016; Ponce-Balbuena et al., 2018; Pérez-Hernández et al., 2018). The gene discussed is SCN5A; the disease is Duchenne muscular dystrophy.