Further studies revealed that replication protein A1 (RPA1) competes with sMAF for binding to Nrf2, activates the cancer-related FOCAD gene, and upregulates focal adhesion kinase (FAK) activity to make NSCLC cells more susceptible to cysteine deprivation-induced ferroptosis, without affecting GPX4 inhibition-induced ferroptosis. This evidence concerns the gene FOCAD and non-small cell lung carcinoma.