Studies conducted by another group using Postn-Cre-mediated myofibroblast-specific deletion of Smad3 and Smad2 found that while deletion of Smad2 temporarily improved cardiac function around 7 days after myocardial infarct (MI) in mice, deletion of Smad3 caused a reduction in cardiac function 28 days after MI (Kong et al., 2018; Huang et al., 2019). This evidence concerns the gene SMAD2 and myocardial infarction.