Considering the major regulatory function of p53 on NOXA and Bax, two p53 and/or p73 downstream target genes, we further selected the p53 double deletion mutant SKOV3 cell line as a model of intrinsic resistance [15]–[17], and the p53-wild type A2780s cell line, which was derived from a untreated patient with primary ovarian carcinoma [17], [18], as a model of intrinsic chemosensitivity, to evaluate the effect of NOXA on the chemotherapeutic efficacy of cisplatin in A2780s and SKOV3 ovarian cancer models in vitro and in vivo. The gene discussed is BAX; the disease is ovarian cancer.