Moreover, the suggestion that this mechanism may be causal in the development of dilated cardiomyopathy in patients that carry a mutation in the 14–3-3 binding motif in PLN may provide rationale for the development of 14–3-3 targeted therapeutic intervention using small molecular stabilizers such as fusicoccin-A or derivatives [31]. The gene discussed is PLN; the disease is dilated cardiomyopathy.