The functional evidence in combination with what was reported in previous animal model studies: the FoxO1 deacetylation affects the function of β‐cells, clearly shows that the HDAC4 mutations are likely pathogenic of childhood hyperglycemia, and the HDAC4 variants cause childhood hyperglycemia with at least limited or even moderate evidence (Strande et al., 2017). This evidence concerns the gene FOXO1 and Hyperglycemia.