Although cardiomyocyte‐specific Fst1 knockout mice (αMHCcre+/− × Fstl1flox/flox) showed a significant decrease (~50%) of Fstl1 in the TAC model (Shimano et al, 2011), there was no appreciable attenuation of Fstl1 protein overexpression in MI model (Fig EV1A). Here, FSTL1 is linked to myocardial infarction.