The current pharmacological mechanism of UA against breast cancer works mainly through the following: the down-regulation of cyclin D1, STAT3, and EGFR, inducing cell cycle and growth arrest [27]; the activation of caspase-9 and caspase-3 through the mitochondrial death pathway to induce apoptosis in MDA-MB-231 breast cancer cells [28,29]; the suppression of p-PI3K, p-AKT, and p-ERK; and enhanced p-FoxO1/FoxO3a expression to significantly decrease migration [30]. This evidence concerns the gene EGFR and breast carcinoma.