## 4 Discussion
These reports prompted the authors to explore the relationship between endometriosis and RPL through the identification of any potential biomarkers common to both the diseases. The present study, in relation to [PERSON] et al. [38], extends the identification of _CTNNB1_, _HNRNPAB_, _SNRPF_, and _TWIST2_ genes as major markers, while the _TWIST2_ gene was identified as the most prominent marker for the exploration of endometriosis and RPL. Although, authors investigated and predicted several parameters reporting challenges in treating the diseases [38]. It is clearly evident from Figure 3 that both the diseases have similar gene expression patterns, thereby providing a clear indication for some common markers for the two diseases. It is also evident from Figure 3 that there exists a clear distinction between the patient and the control groups of each dataset in terms of the expression profiles of the genes. This observation partially supports the idea that the above-mentioned 207 genes may be considered as signatory markers for both EM and RPL. It is clearly evident from Table 2 that the _TWIST2_ gene has the highest fold change value from both the EA and NA analyses. This observation clearly indicates that _TWIST2_ has a significant role to play as a potential diagnostic marker for endometriosis-based recurrent miscarriages. _TWIST2_ has a very important role to play in reproduction. The _TWIST2_ gene is proved to play a very significant role in embryo implantation in mice. Embryo implantation is a very important event for a successful pregnancy. Suppression of the _TWIST2_ gene impaired the embryo implantation by suppressing endothelial-mesenchymal transition (EMT) during embryo implantation [39]. A recent clinical study reported Setleis syndrome in a child with a novel mutation in the _TWIST2_ gene [40]. Another study in 2014 by [PERSON] et al. showed that haploinsufficiency of _TWIST2_ results in reduced bone formation [41]. [PERSON] et al. highlighted _TWIST2_ as a molecular switch during gene transcription [42]. Furthermore, sequestration of E-proteins by increased TWIST2 levels functions to inhibit muscle-specific gene activation [42; 43; 44]. TWIST2 requires Histone Deacetylases for Myoblast Determination Protein 1-Mycocyte Enhancer Factor 2 inhibition [43]. _TWIST2_ is also known to regulate osteoblast differentiation, however its involvement occurs temporally after TWIST1 [41; 45]. The transcription factor RUNX2 is considered a master regulator of the osteogenic program due to its indispensable role in the regulation of most of the genes that give rise to the mature osteoblast phenotype [41; 46]. Both TWIST1 and TWIST2 can also regulate RUNX2 at the protein level by physically interacting with RUNX2 and inhibiting its ability to bind DNA [41; 46]. TWIST2 also acts as an important key negative regulator of myeloid lineage development, as manifested by marked increases in mature myeloid populations of macrophages, neutrophils, and basophils in TWIST2-deficient mice [41; 47]. Therefore, on converging our findings with the above-mentioned published investigations, it is clearly evident that downregulation of the _TWIST2_ gene may have a very potent role in early embryonic developmental events, rendering it as a potential clinical marker for endometriosis based RPL. Another gene, _CA XII_ (Carbonic Anhydrase XII), also has a high log fold change value, as evident from Table 2. _CA XII_ has been found to have prominent expression during mouse embryonic development [48]. However, in this article, we did not focus on other genes in Table 2 since, on overlapping our intersected gene list from EA and NA output with the Geo2R results, only the _TWIST2_ gene was found to be in common. In other words, only the _TWIST2_ gene was found to be present in all the three analyses and therefore was considered to be an important clinical marker. In the case of protein-protein interaction analyses, the top three genes participating in the network were _SNRPF_, _CTNNB1_ and _HNRNPAB_, based on their degree of centrality.