“…Genetic susceptibilities to NTDs in maternal genes related to glucose metabolism have been demonstrated in human studies (Davidson et al, ; Suazo et al, ). The maternal nonsynonymous coding variants HK1 rs748235, LEPR rs1137100, and GLUT1 rs2229682, and the intronic variants LEPR rs2071045 and TCF7L2 rs3814573 may be associated with NTD susceptibility among the American, Irish, and Chilean populations (Davidson et al, ; Carter et al, ; Lupo et al, ; Suazo et al, ). Evidence suggests that abnormal glucose homeostasis is also attributable to genetic variants in other genes encoding proteins such as glucokinase regulator ( GCKR ), IGF‐II mRNA‐binding protein ( IGF2BP ), methylthiotransferase family members ( CDKAL1 , CDKN2A/B ), hematopoietically expressed homeobox protein ( HHEX ), transcription factor ( TCF ), ion channel proteins ( KCNQ1 , KCNJ11 ), and fat mass and obesity‐associated protein ( FTO ) (Wu et al, ; Yajnik et al, ; Liu et al, ; Qi et al, ; Bi et al, ; Shu et al, ; Cui et al, ; Ling et al, ; Sim et al, ; Bao et al, ; Li et al, ; Murata‐Mori et al, ).…”