While current thinking generally aligns with amyloid and tau CSF markers becoming abnormal earlier in the disease cascade than amyloid and tau PET markers,77-79 some conflicting reports suggest similar or higher prevalence of PET+/CSF− in comparison with PET−/CSF+.56,80-82 Further, there are conflicting reports on the distribution and density of flortaucipir binding with different CSF and PET profiles.83,84. The gene discussed is MAPT; the disease is amyloidosis.