Although these pieces of evidence suggest tumor-suppressive functions of MARK3, there is no consensus on whether MARK3 is an oncogene or a tumor suppressor gene; additionally, there is no reliable study describing cancer type-specific dysregulation of MARK3. Given that our analysis identified that downregulation of MARK3 is significantly associated with poor clinical outcomes (Fig. 1e) and platinum-resistant status in patients with HGSOC (Fig. 1f), we hypothesized that MARK3 acts as a tumor suppressor gene and offers a promising therapeutic opportunity. The gene discussed is MARK3; the disease is neoplasm.