These findings implicate these hnRNPs and suggest the involvement of widespread mis-splicing events in the pathogenesis of sporadic FTLD and highlight the need for further investigations to determine whether they contribute to the distinct pathomechanisms increasingly recognized across the ALS-FTLD continuum, as well as to assess their potential as targets and/or proximal markers of TDP-43 dysfunction. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.