Noticeably, an exception, SPP1 was among the top genes driving the shift along the disease axis from the genetic mouse models of AD, was exclusively upregulated in the iPSC-microglia treated with LPS+IFN-γ at both 24 and 28 h, has increased expression in two different studies of post-mortem human AD microglia (Grubman et al., 2019; Mathys et al., 2019) and is characteristic of the ARM subtype (Sala Frigerio et al., 2019). This evidence concerns the gene SPP1 and Alzheimer disease.