Moreover, reduced CV and AP duration coincided with a significant reduction in expression of IGF-1 to pro-adipogenic factors, and these arrhythmia substrates were lessened by the IGF-1 treatment [62], suggesting that enhanced adipogenic signaling via IGF-1 signaling may play an important role in the formation of arrhythmia substrates in ARVC. This evidence concerns the gene IGF1 and cardiac arrhythmia.