Inhibition of FUNDC1 enhances the sensitivity of cancer cells to ionizing radiation and cisplatin, suggesting its involvement in therapeutic resistance.294 Conversely, in hepatocytes, FUNDC1 silencing leads to the accumulation of dysfunctional mitochondria, release of mtDNA, overactivation of caspase-1, and excessive IL-1β production, thus promoting the initiation and progression of HCC.295 These opposing outcomes emphasize the need to evaluate the context-dependent role of mitophagy in cancer development. This evidence concerns the gene IL1B and cancer.