Second, since the summary‐level GWAS data for insulin resistance phenotype were not currently available, we maintained the use of the 53 IVs for insulin resistance phenotype and applied all the IV SNPs based on fasting insulin as a surrogate in MVMR, which might not capture full information on the mediating role of insulin resistance in the causal pathway from sarcopenia‐related traits to cardiometabolic diseases. This evidence concerns the gene INS and Insulin resistance.