The strong enrichment of TDP‐43 interactors and other causal genes for ALS within this module further supports a strong association of M2 with the ALS/FTD spectrum and implicates other novel members of this module as having critical roles in TDP‐43 biology that potentially influence TDP‐43 aggregation or other pathological processes (i.e., microglial‐directed neuroinflammation) inherent to ALS and FTD etiology. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.