In the pathogenesis of arrhythmias observed in ACM that result from genetic mutations affecting the desmosomal cell–cell adhesion complex, particularly the desmoglein-2-W2A mutation, it has been reported that aberrantly activated αVβ6 integrins engage with LAP, leading to the dissociation of the TGF-β1-LAP complex [116]. The gene discussed is TGFB2; the disease is Arrhythmia.