Porcine induced pluripotent stem cells (piPSCs) have significant biomedical and agricultural applications andhave been developed by several laboratories worldwide.Each piPSC line has shown varying levels of heterogeneityin morphology,self-renewal and pluripotency.Thus,questions have been raised pertaining to incompletereprogramming of piPSCs,the plasticity of these cells and the necessary gene regulatorynetworks that are needed to maintain pluripotency.To address these questions and to better understand themechanism of porcine cell reprogramming,we analyzed the transcriptional profiles of porcine iPSC lines usingAffymetrix GeneChip Porcine Genome Array.Our results demonstrated that cell surface proteins of EpCAM(epithelial cells adhesion molecule) and Rexl were significantly upregulated in complete reprogrammed porcineiPSCs,but not in partially reprogrammed cells,suggesting that these genes could be markers for evaluating porcinecell reprogramming.We analyzed gene expression levels of the six key developmental signaling pathways,including JAK-STAT,NOTCH,TGF-b,WNT,MAPK and VEGF.These results demonstrate that the coretranscriptional network to maintain pluripotency and self-renewal in pig may be different from mouse and human.Pig iPSCs lacked expression of specific naive state marker,but expressedunregulated primed state markers.The global networks of pig iPSCs were dominated byhighly connected genes such as POUSFI,LIN28A,DNMT3b,ERK and MAPK,which are possibly critical indetermining the fate of iPSCs.Dlkl-Dio3 domain was silenced in piPSCs as previously seen in mouse and humaniPSCs,which is a likely cause of low instances of chimeric and cloned offspring.Our analysis provides afundamental resource for better understanding of the complex genetic network that maintains pluripotency in thepig.This comparative study with mouse and human may facilitate the derivation of iPS lines from pig moreefficiently.