Activation of FCGR2B (Fcγ receptor IIb, CD32) suppresses excessive pruning via BTK (Bruton’s Tyrosine Kinase) inhibition and INPP5D (Inositol Polyphosphate-5-phosphatase D, SHIP1)-mediated PIP3 hydrolysis, while FCGR3A (Fcγ receptor IIIa,CD16) promotes microglial proliferation and exacerbates synaptic stripping in multiple sclerosis models [77]. Here, BTK is linked to multiple sclerosis.