We did detect overall, non-microglia-enriched differentially expressed genes in the C9orf72 iPSC-MG (Figure 2), including the downregulation of formyl peptide receptor 3, Fpr3. While little is known about the role of Fpr3 in microglial function and activation, its paralog Fpr2 has been implicated in inflammatory responses to Aβ plaques in AD (Le et al., 2001; Tiffany et al., 2001; Cui et al., 2002; Ries et al., 2016). Here, FPR2 is linked to Alzheimer disease.