Recently, Iwahara and colleagues demonstrated that both Aβ-stimulated primary cultured microglia and microglia in a APPswe/PS1dE9 transgenic mouse model of AD expressed SOCS3; they further revealed that SOCS3 was involved in the switch to an activated microglia phenotype (Iwahara et al., 2017), suggesting a potential role for SOCS3 in AD, especially in AD-related neuroinflammation. This evidence concerns the gene SOCS3 and Alzheimer disease.