Considerable evidence has accumulated in the past decade that ultraviolet light contributes to the development of cortical cataract, one of the primary forms of maturity onset cataract worldwide. The long-term goal of cataract research has been to develop strategies aimed at preventing or delaying this disease which ranks as a leading cause of legal blindness. This review is limited to the view that UV, especially in the UVB region, contributes to the pathophysiology of maturity onset cataract. The idea is developed that UVB, like so many other insults, leads to calcium elevation in the lens cortex where opacification typically develops. The calcium hypothesis is introduced and discussed in terms of UVB targets and its evolution is explored to account for new findings that demonstrate UVB impairs the calcium signalling process in human lens epithelial cells.