JNK participate in the MAPK family, that is crucial for cellular functions in eukaryotic cells. Each pathway is preferentially employed by different sets of stimuli, thereby allowing cells to response to numerous divergent inputs in a manner. Recently, groups of researches histone deacetylase inhibitors have indicated the significance of MAPK in characteristics of ectopic endometrial cells and individual eutopic. And the survival and enhanced pro-liferation of eutopic or ectopic endometrial cells from endometriosis patients have already been established to correlate with high rate of MAPK phosphorylation. The JNK protein kinases are collectively known as anxiety activated MAP kinase, and secured by three distinct genes. JNK2 and jnk1 are ubiquitously expressed, while JNK3 is precisely expressed in the mind. JNK phosphorylation and activation occur in a reaction to a number of developmental, environmental, and inflammatory stimuli. Within the canonical JNK pathway, activated JNK functions to phosphorylate the transcriptional activation domain of c Jun, which then constitutes the activator protein 1 transcription factor with c Fos. Therefore, G-protein cou-pled receptors manage Carcinoid MAPK signaling pathways that end in the appearance of particular reaction genes involved with cell proliferation, attack and apoptosis. It might better reveal the role of JNK in IDO1 regulated ESCs, because the regulatory factors such activator protein 1 was on the individual IDO gene promoter region. As it is an effective, mobile permeable and selective inhibitor of JNK because JNK has been shown to be necessary for IDO1 expression, we used SP600125. JNK3 and it comJNK2, demonstrating over 300 fold greater selectivity for JNK. Endometriotic cells are identified with improved growth potency and lower susceptibility to reversible HCV protease inhibitor apoptosis. Nevertheless, SP600125, the blocker of JNK, leaded to the inhibitory action in growth and survival, while provided higher level of apoptosis, along with the expression of p53 in IDO1 overexpressing ESCs. The role of apoptosis within the physiopathology of endometriosis is increasingly obvious. It could be initiated by extracellular and intracellular death indicators that raise p53 protein expression. Facts for p53 as a sign of anomalous apoptosis in endometriosis has been accumulating, specially in ovarian endometriosis. And tests also suggested that JNK pathway is associated with inhibition of p53 in human. Equally, our findings suggest that IDO1 could downregulate the expression of p53, together with ESCs apoptosis through JNK pathway. Survivin has correlated with apoptosis and invasive phenotype of endometriotic tissues, and also been revealed to participate in the endometriosis. It’s been defined to be managed largely through the Raf 1/MEK/ERK pathway in human cells but perhaps not JNK pathway, indicating that increase of survivin in endometriotic tissue may as a result of other factors instead of IDO1.