Under conditions of cellular stress, nuclear levels of phosphatidylinositol-5-phosphate (PI5P) increase. Type I phosphatidylinositol 4,5-bisphosphate 4-phosphatase TMEM55B translocates to the nucleus under stress via an unknown mechanism (Zou et al. 2007) and generates PI5P from the PI(4,5)P2 substrate. The level of PI5P in the nucleus is kept low because of the phosphatidylinositol-5-phosphate 4-kinase activity of nuclear PIP4K2 dimers, mainly dimers containing PIP4K2B (Ciruela et al. 2000). Under conditions of cellular stress, nuclear PIP4K2B is phosphorylated and inactivated by p38 MAP family kinases (Jones et al. 2006).