Importantly, by using the same SPLICS approach, we observed that MERCs density was not significantly perturbed by overexpressing either WT or ALS-related Q331K mutant TDP-43, which led to TDP-43 accumulation in cytotoxic inclusion bodies [63], thereby further suggesting a loss-of-function contribution of TDP-43 in MERCs disruption. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.