While familial studies investigating “lone” AF due to SCN5A have yielded conflicting results regarding pathogenicity [43,44], more recent data suggest that genetic variation in the nearby SCN10A regulates SCN5A expression [45], with alleles associated with prolonged PR interval reducing SCN5A mRNA levels in a dose dependent manner, consistent with our findings. The gene discussed is SCN5A; the disease is atrial fibrillation.