Abnormal RNA homeostasis is increasingly implicated in the pathophysiology of ALS/FTD, consistent with the functions of TDP-43 and FUS in regulating RNA splicing and transport (Polymenidou et al., 2011; Tank et al., 2018). In the transgenic SOD1G93A rat, differences in the number of genes involved in transcription, RNA metabolism, RNA binding and splicing, and regulation of translation, were evident between neuronal populations located in the oculomotor/trochlear nucleus, the hypoglossal nucleus and the lateral column of the cervical spinal cord (Hedlund et al., 2010). These results therefore suggest that RNA homeostatic processes are involved in the differential vulnerability of specific subtypes of MNs in ALS. However, further studies in this area are required to investigate this possibility, particularly in relation to TDP-43 and FUS.