In this study, we investigated the effect of MA on the viability of lung cancer cells and organoids and found that MA promoted the sensitivity of KRAS-mutated lung cancer cells to osimertinib through ROS inhibition of the RAS-ERK pathway and increased the sensitivity of osimertinib-resistant lung cancer cells to osimertinib by mitochondrial Ca2+ overload induced ferroptosis. This evidence concerns the gene KRAS and lung cancer.