In particular, we outline our observations demonstrating that TYROBP deficiency in mouse models of AD-related proteinopathies sustains normal learning behavior and electrophysiological functions even in the face of robust amyloidosis or tauopathy and that TYROBP pathways may act, at least in part, via complement-mediated and/or ERK-related pathways. The gene discussed is TYROBP; the disease is proteostasis deficiencies.