A comparison of our RNA sequencing results with that of the previously published dataset by Zhang et al., has identified a significant number of genes common and differentially expressed in both sets. This suggests that common pathways and molecular mechanisms are operating in association with the aneuploidies, notwithstanding the background cell types in which the experiments have been performed. Though some of the genes shown to differentially express in the present analysis, is shared with previous studies, one of the caveats of our analysis is that it is confined to differentiated cells, rather than in-vivo models. Thus our analysis precludes the potential explanation of specific genes responsible for PI-103 lethality in 45,X fetuses. Turner individuals exhibit an array of clinical phenotypes including osteoporosis, short stature, Diabetes mellitus Type II and gonadal failure. The most accepted hypothesis for Turner phenotypes is the haploinsufficiency of X linked genes like ribosomal protein S4, X-linked, zinc finger protein, X-linked and short BAY-60-7550 stature homeobox. Previous studies on human embryonic stem cells and iPSCs show that X monosomy has a global effect on gene expression, which may be a possible cause for early lethality in most 45,X individuals. We have identified four pseudo-autosomal genes that are expressed at significantly higher levels in 46,XX cells. Haploinsufficiency of ZFX/Y, RPS4X/Y has been thought to be associated with the Turner syndrome. DEAD box helicase 3 X/Y gene family is believed to be involved in embryogenesis, spermatogenesis, cellular growth and division while PRKX/Y encodes a protein kinase which may be related to macrophage and granulocyte maturation. Interestingly, all four of these genes have almost no expression in the 45,X karyotype. Our analysis identified a subset of differentially expressed genes that are associated directly or indirectly with bone metabolism. This potentially suggests a biologically plausible explanation for the high incidence of osteoporosis, which has been one of the characteristic clinical observations in Turner syndrome. One of the genes associated with bone mineralisation, bone morphogenetic protein 2, was found to be down regulated in 45,X cells.