Further analysis of tumors by IHC and western blot revealed that in tumors from mice with E2 supplement the expression of p-4Ebp1, p-mTor, and p-Gsk3β was clearly reduced by AZD5363 treatment relative to vehicle treatment (Fig. 6e and Additional file 8: Figure S8D), confirming the role of AZD5363 in inhibition of the estrogen-induced Akt pathway in Brca1-deficient tumor progression. Here, BRCA1 is linked to neoplasm.