Based on these data, Guo et al. proposed that FLASH-RT preserved mitochondria function of normal lung fibroblasts but not cancer cells through the induction of the phosphorylated form of dynamin-1-like protein (p-Drp1), while CONV-RT led to dephosphorylation of the p-Drp1 and induced Drp1 to be aggregated into mitochondria, which ultimately caused mitochondria fission and cell necrosis [211]. The gene discussed is DNM1L; the disease is cancer.