Moreover, previous studies have reported CCNY as an inhibitory regulator for LTP [11], which has been assumed as a cellular model for learning and memory, and the altered levels of several cytokines in memory-deficit Alzheimer’s disease (AD) mouse model [31] that led us to further validate several genes (Ccl2, Ccl7 and Cxcl1; S2 Table) belonging to chemokine signaling pathway in S3a Fig and additional cytokine genes (Ccl3, Ccl5 and Ccl11) reported in the cytokines-AD study [31] (Fig 5). The gene discussed is CCNY; the disease is early-onset autosomal dominant Alzheimer disease.