This notion would be supported by the development of severe hypomethylation of the PLAGL1:alt-TSS-DMR leading to transient neonatal diabetes mellitus and MLID in patients with ZFP57 pathogenic variants [3], because the postzygotic methylation imprint of the PLAGL1:alt-TSS-DMR is preserved primarily by ZFP57 [4, 5]. Here, ZFP57 is linked to neonatal diabetes mellitus.