Since our data indicate that TGM2 deficiency causes reduced synapse phagocytosis, enhanced expression of postsynaptic density protein PSD‐95 and down‐regulated expression of complement (Cq1a and C1qb), it will be interesting to investigate whether blocking the microglial Tgm2 pathway has a therapeutic potential for synapse damage and loss in the context of neurodegenerative diseases. The gene discussed is C1QB; the disease is neurodegenerative disease.