Accumulating evidence has demonstrated that hypoxia is strongly implicated with activation of AKT signaling in a variety of cell types (51–53), and IL-17 can exert tumor-promoting effects through activation of the AKT pathway (54–56), which prompts us to consider whether CRISP3 drives the pro-carcinogenic progression through activation of the IL-17/AKT signaling axis in BC cells. The gene discussed is AKT1; the disease is neoplasm.