TYROBP and tauopathy: Despite the fact that similar results can be obtained when tauopathy is modulated with either a deficiency of TYROBP or a deficiency of TREM2, a possible explanation for the improvement in behavior and synaptic plasticity is the alteration of the complement system, which is disrupted by Tyrobp deletion, but in our study, not by Trem2 deletion, contrary to the report by Leyns et al. [32].