Disease and Disorders: NUMT insertion into the genome can be problematic. Transposition of NUMTs into genome has also been associated with human diseases. De novo integration of NUMT pseudogenes into the nuclear genome has an adverse effect in some cases, promoting various disorders and aging. MtDNA integration into coding genes in the germline cells has dramatic consequences for embryo development and, in many cases, is lethal. Few NUMT pseudogenes associated with diseases are found within exons or at the exon–intron boundaries of human genes. For example, the patients with mucolipidosis syndrome inherit a mutation caused by insertion of a 93bp fragment of mitochondrial ND5 into exon 2 of the R403C mucolipin gene. This is the first case of a heritable disorder due to the NUMT insert. Despite the small treatment group, Stem Cell transplant found to be effective and lysosomal enzyme levels seemed to normalize after transplant in at least one case. The Pallister–Hall syndrome, a developmental disorder, in another example, where a functional disorder of a key developmental gene results from a "de novo" insertion of a 72bp mtDNA fragment into "GLI3" exon 14 in chromosome 7, which results in central and postaxial polydactyly, bifid epiglottis, imperforate anus, renal abnormalities including cystic malformations, renal hypoplasia, ectopic ureteral implantation, and pulmonary segmentation anomalies such as bilateral bilobed lungs. A splice site mutation in the human gene for plasma factor VII that causes severe plasma factor VII deficiency, bleeding disease, results from a 251-bp NUMT insertion. As the last known example, a 36-bp insertion in exon 9 of the USH1C gene associated with Usher syndrome type IC is the NUMT. No certain curse has yet found for Usher syndrome, however, a current clinical study on 18 volunteers is taking place to determine the influence of UshStat both in a short and a long-term period. This study has been started in September 2013 and is estimated to be done by October 2023.