Pluripotent stem cells have the ability to proliferate extensively in vitro while also possessing the potential to differentiate into various cell types, offering promising prospects for regenerative medicine. However, human bodies possess the capability to recognize self-tissues from foreign ones, leading to immune rejection when foreign cells are transplanted. Additionally, methods such as direct creation of human embryonic stem cell lines or nuclear transfer require use of early human embryos or eggs, raising ethical concerns. This has placed human embryonic stem cell technology at a bottleneck in both regenerative medicine and clinical applications. The breakthroughs in mouse-induced pluripotent stem cells (iPS) in 2006 and human iPS cells in 2007 provided an in vitro culture method for obtaining iPS cells derived from patients’ own somatic cells. This not only avoids autoimmune rejection but also sidesteps ethical issues, offering a new approach to obtaining embryonic stem cells with the patient’s genetic background and ushering in a new era for regenerative medicine. Nevertheless, until the mechanisms behind iPS cell formation are fully understood, the safety of their clinical application will remain a major constraint on the use of somatic cell reprogramming technologies. Existing research indicates that iPS cell formation is primarily governed by epigenetic regulation, but there are few studies on the interactions between epigenetically relevant proteins and transcription factors in this process. This project focuses on studying the epigenetically related molecules involved in iPS cell formation and their specific interactions. It also delves into the specificity, functions, and formation mechanisms of these complexes, providing theoretical foundations and practical strategies to ultimately elucidate the molecular mechanisms of iPS cells, improve their efficiency, and ensure their safe clinical use.