The prioritized genes by GWAS indicated several potential mechanisms of DD onset including dysregulated intestinal wall structure.[6–8] For example, EFEMP1 (epithelial growth factor-containing fibulin extracellular matrix protein 1) encodes an extracellular matrix (ECM) protein, and EFEMP1 knockout mice are susceptible to inguinal hernias.[7] Consistently, our study suggested that, although less prioritized, EFEMP1 protein might be a protective factor for DD. The gene discussed is ECM1; the disease is dentin dysplasia.