Chromosomal loss in trisomy to generate a disomic fetus can cause confined placental mosaicism and/or fetoplacental mosaicism. After trisomy rescue event, there is a risk of fetal uniparental disomy (UPD). The phenotypic consequences of UPD for several chromosomes are still unknown or poorly understood. In this study, we performed whole genome sequencing based NIPT (G-NIPTä) in 1,000 high risk Korean pregnancies and we have detected five cases of other chromosomal trisomies except chromosomes 21, 18 and 13. Chromosomes involved were 7 (1case), 8 (1 case), 16 (1 case) and 20 (2 cases). All three trisomy cases involving chromosomes 7 and 20 were investigated invasively for the presence of UPD. One case of trisomy 7 and one case of trisomy 20 showed normal karyotype at amniocentesis, respectively. However, 1 case of trisomy 20 revealed to have low level of mosaicism of trisomy 20 (47,XX,+20[2]/46,XX[40]) at amniocentesis. To rule out UPD, we performed chromosomal microarray from both amniotic fluid and maternal gDNA in all the three cases. We found 30Mb homozygosity spanning the centeromere in amniocentesis of the low level mosaic 20 case. This finding suggests nondisjunction error happened at meiosis. Then, by comparing all the SNPs of involved chromosomes between mother and fetus, maternal or paternal UPD can be decided. The low level mosaic 20 case can be diagnosed to have maternal UPD 20 and others didn't show any UPD pattern. Recently, maternal UPD 20 has been suggested as a new imprinting disorder with intrauterine growth restriction, short stature and prominent feeding difficulties with failure to thrive. To best of our knowledge, two cases of UPD were detected by following discordant NIPT and invasive testing which were a case of UPD 21 and a case of UPD 15 with fetal mosaicism. From this study, we showed the potential use of NIPT for the detection of UPD, especially when the trisomies of specific chromosomes with imprinting syndromes are detected by NIPT.