Given our findings that profibrotic SPRR1A is an important functional target of miR-150 in whole mouse hearts (Figs. 1–6 and Supplementary Figs. 1–3) and HCFs (Figs. 7, 8, Supplementary Figs. 7–9, and Supplementary Figs. 11, 14) and that SPRR1A was regulated by miR-150 by direct interaction [13], future targeted treatment options based on SPRR1A could be considered in MI patients with decreased levels of miR-150. Here, SPRR1A is linked to myocardial infarction.