It was also proved that matrix-detached epithelial and cancer cells cluster spontaneously through a pathway involved with Nectin-4 (also known as cell adhesion protein PVRL4), the process of which sustains GPX4 expression and buffers against lipid peroxidation by stimulating the PVRL4/α6β4/Src axis signal pathway (Brown et al., 2018). This evidence concerns the gene GPX4 and cancer.