STeerING PI4P for innate immune activation

STING transverses the endoplasmic reticulum (ER), Golgi, and endosomal compartments before its degradation within the lysosomes. In this issue of Immunity, Fang et al. demonstrate that the enrichment of cholesterol and sphingomyelin in the trans-Golgi network and endosomes mediated by the ARMH3-PI4KB-PI4P pathway plays a pivotal role in STING activation under cGAS-dependent and -independent conditions.