For instance, tumor suppressor protein p53, which promotes cellular senescence and apoptosis has been identified to inhibit pluripotency.7 Indeed, in ovarian cancer, loss of p53 expression or function due to genetic mutation or post-translational modifications is often associated with hyper-proliferation, apoptosis resistance and stemness.8, 9 To date, numerous post-translational modifications including phosphorylation, acetylation, methylation and ubiquitylation have been reported to modulate p53 functions in tumorigenesis.10 Here, TP53 is linked to ovarian cancer.