Therefore it is reasonable to hypothesize that, although the amino acid sequence of human and murine tau surrounding this epitope is divergent, 12A12mAb is more likely to recognize the newly generated, sequence- and structural-based immunoreactive determinants whose formation requires pathological truncation occurring under Alzheimer’s disease conditions at D25 residue both in human and rodent tau (Rohn et al., 2002; Corsetti et al., 2008; Quinn et al., 2018; Amadoro et al., 2019). The gene discussed is MAPT; the disease is Alzheimer disease.