STIM1 and transient myeloproliferative syndrome: Since in non-excitable cells DES blunts SOCE by restraining STIM1 access to ORAI1, it may act as a cytoskeletal controller of intracellular Ca2+, and loss of DES control over STIM1 diffusion along the endoplasmic reticulum has recently been hypothesized in the pathogenesis of TAM (37).