The HUSH complex plays a pivotal role in linking retrotransposon silencing with innate immunity, primarily through its control of L1 expression and the subsequent mitochondrial anti-viral signaling protein (MAVS)-dependent sensing of L1 RNA.18,69 In the context of cancer, disruptions to the HUSH complex leading to L1 dysregulation have been shown to trigger innate immune pathways, resulting in the death of cancer cells.19,69 We speculated whether the cell death observed during the transition from Tasor KO ESCs to EpiLCs could be due to an innate immune response. The gene discussed is MAVS; the disease is cancer.