The strongest signal we observed was for inversions affecting CTCF-only regions, potentially implicating disrupted chromatin looping in the underlying pathogenesis of PUV and raising the interesting possibility that non-specific perturbation of long-range regulatory networks or TADs could manifest as PUV, perhaps due to sensitivity of integration of the mesonephric duct into the posterior urethra to even minor abnormalities of gene expression. This evidence concerns the gene CTCF and posterior urethral valve.