These data suggest that tSTMN2 and other cryptic exon-containing transcripts normally suppressed by TDP-43 are sensitive markers of TDP-43 loss of function, thus providing a rationale to study their possible utility as biomarkers for distinguishing patients with FTD caused by TDP-43 proteinopathy vs. tauopathy—an endeavor of great importance to the FTD field. The gene discussed is TARDBP; the disease is frontotemporal dementia.