Given that most of the ROSmiRs are directly or indirectly regulated by p53 [8] (Figure 1E), and p53 is frequently mutated during the early and later stages of high-grade serous carcinoma, the role of p53 independent ROSmiR, such as miR-182 expression and its function in FTE cells, seems to be pivotal when p53 is partly or completely inactivated. This evidence concerns the gene TP53 and serous adenocarcinoma.