Conversely, analysis of variants of the β-catenin destruction complex genes AXIN2 and glycogen synthase kinase 3 beta (GSK3B) in NSCLP families across multiple populations identified intronic SNPs that contribute to orofacial clefts (Letra et al., 2009; Letra et al., 2012; Vijayan et al., 2018) (Table 1), suggesting that excessive WNT/β-catenin signaling also contributes to CLP pathogenesis. Here, GSK3B is linked to orofacial cleft.