To determine whether TDP-43 APA of MARK3 could contribute to disease pathogenesis in ALS/FTD and AD, we evaluated the effect of TDP-43 knockdown on MARK3 phosphorylation of tau at S262, a well-established MARK3 phosphorylation site with potential pathophysiological implications, because tau phosphorylation at this residue, which is located within a tau microtubule-binding site (43), can reduce the microtubule-stabilizing properties of tau and antagonize microtubule tracking at the plus end by disrupting interaction between end-binding protein 1 and tubulin (44, 45). This evidence concerns the gene TARDBP and Alzheimer disease.