Memory of mammalian barrier tissues has been recognized as involving cooperative functions ascribed to epithelial, immune, neuronal, and stromal cells, among others.65–67 Studies of epidermal stem cells have shown that the inflammatory memory response to imiquimod encompasses activation of STAT3 as a stimulus-specific inflammatory response and formation of JUN/FOS complexes to maintain memory.46 The present results mirror those findings by identifying STAT1 as an osimertinib stimulus-selective inflammatory response in NSCLC cells. Here, JUN is linked to non-small cell lung carcinoma.