JNK fit in with the MAPK family, that will be critical for cellular functions in eukaryotic cells. Each pathway is preferentially employed by distinct sets of stimuli, thereby allowing cells to reaction to multiple divergent inputs in a manner. Recently, clusters of studies MAPK family have indicated the importance of MAPK in features of human eutopic and ectopic endometrial cells. And the survival and increased pro-liferation of eutopic or ectopic endometrial cells from endometriosis patients have been confirmed to correlate with high rate of MAPK phosphorylation. The JNK protein kinases are collectively known as stress activated MAP kinase, and secured by three different genes. JNK1 and JNK2 are ubiquitously expressed, while JNK3 is precisely expressed in the brain. JNK phosphorylation and activation occur in response to various environmental, developmental, and inflammatory stimuli. Within the canonical JNK pathway, activated JNK acts to phosphorylate the transcriptional activation domain of c Jun, which in turn constitutes the activator protein 1 transcription factor with c Fos. Consequently, G-protein cou-pled receptors control Eumycetoma MAPK signaling pathways that end in the appearance of certain reaction genes involved in cell growth, attack and apoptosis. It might better describe the role of JNK in IDO1 regulated ESCs, considering that the regulatory elements such activator protein 1 was situated on the individual IDO gene promoter region. Because JNK has been proven to be necessary for IDO1 expression, we used SP600125 since it is a potent, cell permeable and selective inhibitor of JNK. It comJNK2 and JNK3, showing more than 300 fold higher selectivity for JNK. Endometriotic cells are identified with improved growth capability and lower susceptibility to Dub inhibitors apoptosis. Nevertheless, SP600125, the blocker of JNK, leaded to the inhibitory activity in growth and survival, while provided greater level of apoptosis, as well as the expression of p53 in IDO1 overexpressing ESCs. The role of apoptosis in the physiopathology of endometriosis is increasingly clear. It could be initiated by extracellular and intracellular death signals that raise p53 protein expression. Evidences for as a marker of anomalous apoptosis in endometriosis p53 is accumulating, specially in ovarian endometriosis. And studies also recommended that JNK pathway is associated with inhibition of p53 in human. Equally, our results suggest that IDO1 could downregulate the expression of p53, together with ESCs apoptosis through JNK pathway. Survivin has also been revealed to be involved in the endometriosis, and correlated with apoptosis and invasive phenotype of endometriotic tissues. It has been defined to be regulated primarily 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 rather than IDO1.