There is extensive evidence that Aβ induces theactivation of JNK in familiar AD mouse models.19,33,34 Moreover, it has been described that Aβ42 ICV injection induces astroglial and microglial activationand, as a consequence, neuroinflammation and neurocognitive impairment.32 In this line, our study reported a significantincrease in pJNK levels after Aβ42 ICV injectionin healthy mice, according to the published literature35,36 and suggesting that pJNK activation is the consequence rather thanthe cause of Aβ accumulation. The gene discussed is MAPK8; the disease is Alzheimer disease.