Many pluripotency factors, including the master transcription factors Oct4, Sox2 and Nanog, and signaling pathways (e.g., β-catenin signaling), are also operative in cancer cells (see Figure above). Owing to the intrinsic connection between pluripotency and tumorigenesis, a number of novel pluripotency transcription factors (e.g., ZFP281, NAC1, PSPC1 and NONO) and epigenetic regulators (e.g., TET1/2) that are important for stem cell maintenance and somatic cell reprogramming are being increasingly recognized for their roles in cancer. We have already established productive collaborations with cancer researchers in studying certain pluripotency regulators and signaling pathways in cancer (e.g., ovarian cancer and leukemia) development (see our publications). For example, we have studied functions of the BTB-POZ transcription factor NAC1, initially discovered in our Nanog interactome studies (Wang et al., Nature 2006), in human ovarian (SKOV3) and cervical (HeLa) cancer cells (Paper-1; Paper-2). We have identified novel Tet2 partners in both ESCs (Guallar et al., Nature Genetics 2018) and hematopoietic cells, the latter of which led to a better understanding of hypermutagenicity of HSPCs in Tet2 mutant hematopoietic cells and animals (Pan et al., Nature Communications 2017). Accordingly, a new direction of our lab research is to employ our well-established proteomic and genomic approaches together with the rich resources of information and reagents from our stem cell studies to facilitate understanding of the pathogenesis of cancers.