Microcephalic osteodysplastic primordial dwarfism type II (MOPD II) and Seckel syndrome, characterized by intrauterine growth restriction, microcephaly, and short stature, represent distinct genetic disorders converging on the genomic stability signaling pathway, with MOPD II arising from PCNT mutations and Seckel syndrome resulting from mutations in CEP63, ATR, CENPJ, NIN, CEP152, and RBBP8 [6,7]. This evidence concerns the gene NIN and Seckel syndrome.