do not use assays that detect neocentromere formations. Although not discussed explicitly in relation to neocentromeres, it is worth noting that the breakage-fusion-bridge cycle involves ring chromosomes too. Particularly, these ring chromosomes involved in breakage-fusion-bridge cycles have a relatively high percentage of prevalence in lipomatous tumors and a lower but still notable prevalence in lung and acute myelogenous leukemia, according to the Mitelman Database. Perhaps further studying of ring chromosomes and diseases, from the perspective of neocentromere formation, may shed light on mechanisms of tumor formation due to chromosome abnormalities. For example, one may question whether the ring chromosomes present in tumors contain a neocentromere following a Class II deletion, because the neocentromere may or may not be present on the ring. As well as autosomes, human neocentromeres have also been observed in sex chromosomes, and correlate with some sex-linked diseases. In 1999, analysis of a neocentromere in the Y chromosome with a constriction site in the amniocytes of a 38-year-old woman, and in her husband and brother-in-law served as experimental evidence that neocentromeres can be stably transmitted through meiosis into the next generation. Not only is the neocentromere viable on a chromosome, it is also sufficient for allowing proper male sex determination. These meiotically transmitted neocentric markers show mosaicism, which many think are due to mitotic instability. However, in contrary, others also think that mosaicism could be developed post-zygotically and hence may not be a result of mitotic instability. Post-zygotic formation happens when the function of the neocentromere is not established at the time of meiotic rearrangement. Another case of mosaicism has been observed in a 15-year-old girl with a neocentric X chromosome. Her clinical features, along with cytogenetic and FISH analyses confirm that this is the first case of a mosaic Turner syndrome involving a neocentromere. During the time of this experiment, only two other cases of neocentric X chromosomes had been observed thus far, making this experiment the third. One of the two previous cases was also confirmed to be Turner syndrome but was not mosaic. An interaction of interest here would be between neocentromeres and the XIST gene, which is responsible for X-inactivation. It has been suggested that the abnormality caused by neocentromeres may account for the selective inactivation of the abnormal X chromosome in this patient. Taking into account that only fewer than 5% of Turner syndrome cases are mosaic, one may consider, likewise with