In conclusion, our study shows that MA is a novel EGFR-TKI sensitizer in KRAS-mutated and osimertinib-resistant lung cancer cells by suppressing the KRAS-ERK pathway and inducing ferroptosis via suppressing NRF2-SLC7A11 axis and mitochondrial Ca2+ overload induced-FTH1 pathways. This evidence concerns the gene EGFR and lung carcinoma.