To gain more insight into the underlying mechanisms of K63 ubiquitination in AD pathology, AD TauO-treated iHEK-Tau cells with K63-linkage overexpression were analyzed for the mechanisms involved in cell survival, inflammatory, and stress response including the mitogen-activated protein kinase (MAPK), protein kinase B (Akt), Janus kinase-signal transducer and activator of transcription (JAK/STAT), nuclear factor-kappaB (NFκB), and transforming growth factor beta (TGFβ) (Figs. 6 and S4, A–E). Here, TGFB1 is linked to Alzheimer disease.