NFκB‐cRel is known to be an osteoblast‐related TF(24) and has been shown to be a crucial factor responsible for impaired bone formation in osteoporosis,(25) whereas AP‐2A has been shown to enhance the osteogenic differentiation potential of MSCs.(27) Thus, further studies using electrophoretic mobility shift assay (EMSA) and/or chromatin immunoprecipitation (ChIP) have the potential to verify TF binding at these SNPs and thus implicate potential roles for these TFs in EPDR1 gene regulation. The gene discussed is REL; the disease is osteoporosis.