Our previous study showed that haplodeficiency of ALK4 alleviated cardiac fibrosis secondary to myocardial infarction and preserved cardiac function [20], and partial inhibition of ALK4 was able to attenuate cardiac fibrosis result from the pressure overload and improve cardiac function [21] through suppressing Smad2/3 activity. This evidence concerns the gene ACVR1B and myocardial infarction.