In WAD, mutations in the last exon of EVC2 may escape NMD and the resulted, more stable EVC2 proteins may have a negative effect by gaining a function or affecting the normal protein (Ibarra‐Ramirez et al., 2017; Shen, Han, Zhang, Zhao, & Feng, 2011; Shi et al., 2016; Valencia et al., 2009). The gene discussed is EVC2; the disease is acrofacial dysostosis, Weyers type.