Due to genome instability, some tumor cells spontaneously produce cGAMP, which is transferred to non-tumor cells; tumor cGAS and host STING were required for antitumor immune responses, supporting the cGAMP transfer model.38,39 So far, gap junctions, SLC19A1, P2X7R, and LRRC8 were reported to transmit cGAMP from cell to cell or from the extracellular region to cells.40–45 Altogether, spontaneous cancer immune surveillance is induced by tumor-derived DNA or cGAMP transferred into host cells (Fig. 2b). Here, LRRC8A is linked to neoplasm.