For example, individuals with MODY caused by mutations in GCK (GCK-MODY) have mild, non-progressive hyperglycaemia present from birth with low risk of complications and typically do not require treatment [40]; individuals with HFN1A- and HNF4A-MODY may achieve excellent control with sulfonylureas [41] or glucagon-like peptide 1 (GLP-1) receptor agonists [42], removing the need for insulin. Here, HNF4A is linked to MODY.