A search of the databases (Wanfang, CNKI, and PubMed) for studies published up to March 31, 2024, using the search terms “SCLA16A2,” “Allan–Herndon–Dudley,” “nonsense,” and “MCT8,” revealed 9 types of nonsense mutations in the SCL16A2 gene resulting in AHDS (Table 1).[5,13,18–23] Despite the absence of a predictive model for genotype-phenotype correlation, AHDS tends to be clinically severe when nonsense mutations cause structural deletion of MCT8 proteins or fail to produce MCT8, resulting in significant hypoplasia or loss of transporter T3 function. This evidence concerns the gene SLC16A2 and Allan-Herndon-Dudley syndrome.