GPX4 and neoplasm: The underlying mechanism uncovered by the present study demonstrated that α9 nAChR was able to activate AKT-, ERK- and STAT3-mediated signaling pathways and suppressed ferroptosis via promoting SLC7A11/GSH/GPX4 and Keap1/Nrf2/HO1 signaling, ultimately supporting the continuous tumor cell growth of TNBC (Figure 7).