GRIN2B and tuberculosis: Causality presently established between synaptic accumulation of GluN2B and the degradation of hippocampal function in TB/DM, challenges the hypothesis that a reduction in GluN2B‐dependent transmission contributes to cognitive aging (e.g., Hara et al., 2018; Wang et al., 2014) and highlights the targeting of the receptor's mobility as a potential alternative therapeutic strategy.