In addition, in the traumatic brain injury (TBI) rodent model, excess IFN-beta was released from the “sick neuron” under the endoplasmic reticulum stress conditions via STING signaling, and enforced activation and pro-inflammatory M1 polarization of microglia, which resulted in secondary brain injury by recruiting more infiltration of peripheral immune cells (Sen et al., 2020). The gene discussed is STING1; the disease is brain injury.