Without the presence of dissolved NaOH or KOH, responsible for the high pH (~13.5) of the concrete pore water, the amorphous silica of the reactive aggregates would not be dissolved and the reaction would not evolve. Moreover, the soluble sodium or potassium silicate is very hygroscopic and swells when it absorbs water. When the sodium silicate gel forms and swells inside a porous siliceous aggregate, it first expands and occupies the free porosity. When this latter is completely filled, if the soluble but very viscous gel cannot be easily expelled from the silica network, the hydraulic pressure rises inside the attacked aggregate and leads to its fracture. It is the hydro-mechanical expansion of the damaged siliceous aggregate surrounded by calcium-rich hardened cement paste which is responsible for the development of a network of cracks in concrete. When the sodium silicate expelled from the aggregate encounters grains of portlandite present in the hardened cement paste, an exchange between sodium and calcium cations occurs and hydrated calcium silicate (C-S-H) precipitates with a concomitant release of NaOH. In its turn, the regenerated NaOH can react with the amorphous silica aggregate leading to an increased production of soluble sodium silicate. When a continuous rim of C-S-H completely envelops the external surface of the attacked siliceous aggregate, it behaves as a semi-permeable barrier and hinders the expulsion of the viscous sodium silicate while allowing the NaOH / KOH to diffuse from the hardened cement paste inside the aggregate. This selective barrier of C-S-H contributes to increase the hydraulic pressure inside the aggregate and aggravates the cracking process. It is the expansion of the aggregates which damages concrete in the alkali-silica reaction.