As a future direction, a hypermorphic mouse model with reduced FAM210A expression, such as a homozygous knock-in of a human mutation (if conserved in mice) or a heterozygous knockout, is more suitable for recapitulating the loss-of-function human mutation or decreased expression in myocardial infarction, thereby confirming the causal effects of decreased FAM210A level in heart diseases. This evidence concerns the gene MIMS1 and myocardial infarction.