Additionally, while the JUNB regulatory network has not been implicated in AD processes, the kinase signaling pathway of its TF binding partner, cJun, has been consistently proven as a regulator of many AD-related phenotypes, such as cognitive impairment, altered synaptic function, glial clearance of Aβ plaques and neuronal death (MacDonald et al., 2013; Sclip et al., 2014; Scopa et al., 2023). The gene discussed is JUN; the disease is Cognitive impairment.