The congenital theory of the etiology of intracranial berry aneurysms has been widely accepted for many years. Review of the supporting evidence indicates that it is not based on sound scientific data but on unscientific and unsubstantiated allegations. There is no evidence of a congenital, developmental, or inherited weakness of the vessel wall. The most plausible explanation is that the aneurysms are acquired degenerative lesions--the effect of hemodynamic stress. The mural atrophy leading to aneurysmal dilatation is an acquired lesion which can be produced experimentally by hemodynamics alone. Hypertension and connective tissue disorders associated with acquired loss of tensile strength of the connective tissues are not essential: they appear to be aggravating rather than causal factors. Occlusion of one or more feeding vessels may enhance the possibility of aneurysm formation at large arterial forks subjected to the augmented hemodynamic stress associated with collateral flow.