While many genes such as Interleukin-1 Receptor Type 1 (Il1r1) and Myd88 form proinflammatory signaling cascades and are upregulated in human AD (Zarezadeh Mehrabadi et al., 2022), reduced Myd88 expression has demonstrated to result in greater cognitive deficits and spatial memory impairment, as well as increased soluble oligomeric amyloid-β in APPswe/PS1 transgenic mice, emphasizing the importance in microglia activation to mitigate AD evolution (Michaud et al., 2011). The gene discussed is MYD88; the disease is Alzheimer disease.