While our findings support the central role of HYBID in cardiac fibrosis, several limitations warrant consideration: (1) The role of HYBID in other cardiac cell types and systemic fibrosis post-MI remains unexplored; (2) validation in alternative models (e.g., pressure overload) and human samples is needed; and (3) only male mice and short-term (≤4 weeks) effects were examined. This evidence concerns the gene CEMIP and myocardial infarction.