ONLINE COVER This week, Gamage et al. show that the deletion of a single amino acid (Glu²⁹⁶) reverses the pathophysiological effects of the disease-associated R304W mutation of the ER Ca²⁺ sensor STIM1 by restoring the intramolecular contacts required for the inactive conformation. The image shows μCT scans of cortical (top row) and trabecular (bottom row) bone in a wild-type mouse (left column), a mouse expressing the R304W mutant (center column), and a mouse expressing STIM1 with both the R304W mutation and Glu²⁹⁶ deletion (right column).