In a recent study, RBFOX2 overexpression in mice, mimicking the RBFOX2 overexpression seen in human DM1 patients, triggered splicing defects in sodium and potassium channels (Kv4.3), which could potentially explain the reduced Ito seen in Homo mice (Misra et al., 2020). This evidence concerns the gene KCND3 and myotonic dystrophy type 1.