FKN-mediated activation of microglia and neuroinflammation has been well reported in case of neurodegenerative disorders, such as Alzheimer’s disease, where the disrupting FKN signaling significantly attenuated amyloid β accumulation due to the increased phagocytic activity of microglia (Finneran and Nash, 2019) and in the case of Parkinson’s disease the inhibition of FKN signaling attenuated α-synuclein aggregation (Thome et al., 2015). Here, CX3CL1 is linked to Parkinson disease.