Bencze et al. (2018) recently reviewed the role of LMTK2 in neurodegeneration. The authors proposed three LMTK2-dependent mechanisms of neurodegeneration: (i) disruption of axonal transport, mediated by aberrant LMTK2-kinesin-1 interaction; (ii) hyperphosphorylation of Tau protein by LMTK2, mediated by cdk5 and GSK3-β; and (iii) regulation of apoptosis by LMTK2 (Bencze et al., 2018). The authors proposed that modulation of LMTK2 expression could be considered as a promising novel therapeutic target for neurodegenerative states, such as Alzheimer disease (Bencze et al., 2018). This evidence concerns the gene LMTK2 and early-onset autosomal dominant Alzheimer disease.