It was suggested that reducing the buildup of hyperphosphorylated Tau could slow down the progression of Alzheimer’s disease [34]: by investigating the connection between Tau phosphorylation and PP-IPs in humanized yeast models of Alzheimer’s, researchers discovered that cells lacking Kcs1 and Vip1 kinases exhibited higher levels of hyperphosphorylated Tau; additionally, disrupting the PP-IP pathway upstream of IP6 resulted in reduced levels of total Tau, but did not decrease the extent of hyperphosphorylation. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.