Ki-67 depletion has also been linked to reduced activity of the Dimerization partner, RB-like, E2F, and Multi-vulval class B (DREAM) complex, which depends on a functional p21 checkpoint.30–32 De Vicente et al. reported more p53-positive cells in OKC epithelium compared to dentigerous and radicular cysts, possibly reflecting overproduction or stabilization of wild-type p53 in response to increased proliferation.3 These findings suggest that OKCs may have impaired tumor suppressor function, contributing to their high proliferative potential—even in comparison to ameloblastomas. The gene discussed is MKI67; the disease is neoplasm.