Recent progress in molecular characteristics of ovarian cancer has helped delineate the origins of carcinogenesis, particularly, a model of tumorigenesis which is based on a dichotomous theory of (1) low-grade or type I ovarian cancer associated with gene stability and multiple isolated mutations and (2) high-grade type II ovarian cancer associated with genetic instability and p53 mutations. This evidence concerns the gene TP53 and ovarian cancer.