However, an early mechanistic study showed biochemical and functional evidence linking ARID1A and TP53 regulation and mutant ARID1A-TP53 mutual exclusivity in a cohort of 77 ovarian clear cell and uterine endometrioid carcinomas, where all ARID1A mutant tumors were TP53 wild-type, and vice versa [22]. The gene discussed is TP53; the disease is endometrial endometrioid adenocarcinoma.