The PI3K/AKT/mTOR signaling pathway is a complex intracellular biochemical cascade that is routinely disrupted in breast cancer and its activation favors cellular growth, proliferation, and survival [33,34]. Ipatasertib and Capivasertib are both pan-AKT inhibitors that are still under consideration for the treatment of mTNBC [35,36]. Both competitively inhibit all AKT isoforms and suppress the phosphorylation of AKT substrates that mediate cellular processes such as mitosis, apoptosis, and glucose or fatty acid metabolism. The gene discussed is AKT1; the disease is breast cancer.