Administration of AZD5363 to creatine-treated hypoxic breast cancer cells mitigated the effect of creatine on activation of AKT-ERK signaling (Fig. 7c), and correspondingly led to decrease of Bcl-2 protein and increase of pro-apoptotic proteins (e.g. Bax and activated (cleaved) Caspase-3) (Fig. 7d), which was echoed by corresponding alteration of hypoxic TNBC cell viability (Figure S6B). The gene discussed is BAX; the disease is breast carcinoma.