Pluripotent stem cells have the ability to proliferate extensively in vitro and possess the potential to differentiate into various cell types, presenting a promising future for regenerative medicine. However, humans have the capacity to recognize self and foreign tissues, and transplanted foreign cells face the challenge of immune rejection. In addition, whether it is through direct establishment of human embryonic stem cell lines or nuclear transfer methods, the use of early human embryos or eggs will inevitably lead to ethical issues, making human embryonic stem cell technology in regenerative medicine and clinical applications a bottleneck. The technical breakthroughs of induced pluripotent stem cells (iPS) from mice in 2006 and human iPS cells in 2007 provided an in vitro cultivation pathway for obtaining patient-derived autologous iPS cells, avoiding not only the problem of autoimmune rejection but also ethical concerns. The proposal of new pathways for obtaining embryonic stem cells with the patient's own genetic background has unveiled a brand-new chapter in the development of regenerative medicine. However, before the mechanisms of iPS cell formation are clearly understood, the safety of their clinical application will severely restrict the use of somatic cell reprogramming technology in clinics. Research has shown that iPS cell formation is mainly a problem of epigenetic regulation, but there are few reports on the interactions between epigenetic-related proteins and transcription factors in iPS cell formation. This project focuses on the study of epigenetic-related molecules in iPS cell formation and their specific interactions, and delves into the specificity, function, and formation mechanisms of these complexes, providing theoretical basis and feasible strategies for ultimately elucidating the molecular mechanisms of iPS cells, improving the efficiency of iPS cells, and ensuring their safe clinical application.