The sporadic phenotypes observed in Dnmt3a2−/−mice, including anophthalmia, hydrocephalus, and hydronephrosis, which reflect profound developmental defects, such as the complete absence of the ureter (hydronephrosis), eye (anophthalmia), and potentially ciliary dysfunction (hydrocephalus), can be attributed to DNA methylation changes caused by the loss of Dnmt3a2 during critical developmental windows, rather than genetic mutations or environmental causes. This evidence concerns the gene DNMT3A and hydronephrosis.