The knockdown of PRIM2 enhanced the sensitivity of NCI-H23 cells to dihydroartemisinin therapy, while the overexpression of PRIM2 had the opposite effect, indicating that dihydroartemisinin induced ferroptosis in lung cancer cells by upregulating the PRIM2/SLC7A11 pathway [25]. The gene discussed is PRIM2; the disease is lung carcinoma.