EGFR and the members of its family have been reported to activate NF-κB via PI3K/AKT signaling, mainly in estrogen receptor negative (ER−) breast cancers [37], while sustained activation of PI3K/AKT, MAPK, and JAK/STAT pathways in aggressive prostate cancers leads to constitutive NF-κB activity through the establishment of a cytokines-mediated autocrine loop and androgen receptor upregulation [38]. The gene discussed is AKT1; the disease is breast carcinoma.