reported that SGC707 does not influence glial cell proliferation, a feature commonly associated with gliosis, suggesting that its effects on neuroinflammation may be mediated indirectly through the modulation of tau pathology.[19a] This finding underscores the robust cascade of downstream effects triggered by alleviating tau hyperphosphorylation, highlighting the therapeutic potential of targeting PRMT3 in tauopathies. This evidence concerns the gene PRMT3 and tauopathy.