Salk Institute researchers tied a key immune paradox to mitochondria and interferon signaling, reporting that chronic type II interferon exposure promotes tumor growth via mitochondrial RNA–induced type I interferon and prostaglandin synthesis. The work, published in Science, explains how a pathway that is initially anti-cancer can shift into a pro-tumor mode under prolonged stimulation. In parallel, a separate study reported metformin’s capacity to ease interferon-driven dendritic cell inflammation in STAT1 gain-of-function disease, published in Cell Death & Disease. Metformin’s effects were linked to rewiring dendritic cell metabolism—an angle that could support repurposing strategies for hyperinflammatory genotypes. Together, the findings reinforce a mechanistic bridge between immune signaling, mitochondrial function, and therapeutic modulation—creating clearer hypotheses for resistance and inflammatory toxicity management.