Other than ECM stability, the successful inhibition of aneurysmal growth by PGG in AAA rat CaCl2 models in vivo is likely due to (i) its ability to be a radical scavenger [12,13,14], (ii) lower inflammatory responses [12,17,21,57,58,59], (iii) acting as a calcium antagonist (blocks inositol 1,4,5-trisphosphate receptors) [60], and (iv) reducing MMP activity [18,19,20,21,58]. Here, ITPR1 is linked to triple-A syndrome.