This suggests that these NSAIDs might operate through multiple underlying biological pathways to lower BC risk, including a direct effect through ER mediated signaling pathways [13, 41], the COX-2 pathway [13, 50], phosphatidylinositol 3-kinase down-regulation [13, 51], B cell lymphoma 2-mediated apoptosis [13, 52], or epidermal growth factor receptor inhibition and p53 acetylation [13, 53]. Here, TP53 is linked to breast cancer.