The underlying mechanism of this effect is that IFNγ is recognized by receptors on the tumor cell membrane, increasing the expression of the transcription factor STAT1, which in turn downregulates the expression of SLC7A11 and SLC3A2, resulting in the inhibition of the GSH/GPX4 axis, and finally sensitizing tumor cells to ferroptosis (Wang et al., 2019). This evidence concerns the gene SLC3A2 and neoplasm.