Numerous biliary proteins as well as non-protein factors influence kinetics of cholesterol crystallisation from supersaturated bile. Cholesterol crystallisation pathways, methods used for quantitative evaluation of liquid-to-solid transition of cholesterol in bile and the classical concept of nucleation defect in pathogenesis of gallstones are reviewed in the first part of this article. The relevance of individual biliary proteins and non-protein factors is discussed in the second part. Finally, a new concept according to which accelerated crystallisation of cholesterol inhibits gallstone growth and protects the gallbladder wall from toxic injury resulting from the increased absorption and accumulation of cholesterol from supersaturated bile is suggested.