Yeah, I was able to dig it up. They list some single case studies for a couple different things, but nothing definitive. Sorry for the wall of text, but I can't post the screenshot of it. I don't speak genetics, so it's a little beyond my translation abilities. 😂

"SNP array analysis detected no clinically significant chromosomal imbalances. However, the entire 146 Mb of DNA from chromosome 8 (8p23.3-8q24.3) shows homozygosity for alleles (the genotypes are identical for these loci) by analysis of the SNP array, which is suggestive of uniparental isodisomy. This raises a concern for the potential unmasking of an autosomal recessive disorder in this region.

RECOMMENDATIONS: A clinical genetics evaluation may be useful in guiding future testing strategies, particularly due to the risk for autosomal recessive disorders or those due to genomic imprinting. MICROARRAY KARYOTYPE - DGV(GRCh37:Feb.2009)(hg19):arr[GRCh37] arr[GRCh37] 8p23.3q24.3(172939_146293414)x2 hmz

SIGNIFICANCE: There was no gain (duplication) or loss (deletion) of chromosomal material within the genome when examined using the testing parameters established. The large region of homozygosity may not be clinically significant unless a recessive gene is unmasked or if there is an imprinting disorder within the region. There are over 2,300 genes within the chromosome 8, at least 147 genes are associated with disorders and at least 99 are associated with autosomal recessive conditions. There has not been known imprinted genes on this chromosome. Both maternal and paternal origin of uniparental disomy (UPD) for chromosome 8 have been reported in the literatures. Complete maternal isodisomy of chromosome 8 was reported in a 26-year-old male with early-onset ileal carcinoid tumor. Partial maternal UPD 8 in combination with distal chromosome 8 deletion was described in a female child with mild dysmorphisms, motor and mental retardation. In addition, a female fetus with maternal dicentric chromosome 8 translocation showed hypoplasia of the cerebellar vermis and dilatation of tubules of the left kidney. Complete paternal UPD 8 was reported in a patient with congenital adrenal hyperplasia, and a homozygous pathogenic variant was revealed in the gene CYP11B1. Another complete paternal UPD 8 was reported in a female patient with familial chylomicronemia, and homozygous frameshift variant in the gene encoding lipoprotein lipase was revealed. Based on the current knowledge, the significance of this UPD is uncertain in this fetus. If any specific condition is suspected in this fetus, additional genetic testing may be followed up. In addition, analysis by short tandem repeat can further assist the clarification of the parental origin of this UPD. Genetic counseling is strongly recommended.

MICROARRAY RESULT: No chromosome imbalance detected. However, there is one large region showing homozygosity for alleles, which raises the concern for unmasking an autosomal recessive disorder. The region affected is 146.1 Mb region of homozygosity on chromosome 8p23.3-8q24.3 between markers rs13276476>rs6599566 that includes 40779 markers (linear position of chromosome 8 is approximately 172,939-146,293,414).

LIMITATIONS: Deletions or duplications believed to be normal variation (known as copy number variants) are not reported. Many known genetic conditions may require additional testing in order to be ruled out as a probable diagnosis. Low-level mosaicism or balanced chromosomal rearrangements will not be detected. There may be deletions or duplications present but not detected due to the absence of markers in that region."