Primary and secondary lens fibres are formed by lens fibre cells, and gap junctions between these cells are vital for maintaining lens transparency. Xiaohua Gong and colleagues (p. 2033) have investigated how mutations in the genes that encode gap-junction subunits(which allow the exchange of molecules between cells) predispose to cataract formation. The gap junctions between lens fibre cells consist of two connexin subunits - α3 (Cx46, encoded by Gja3) and α8 (Cx50,encoded by Gja8). The researchers have identified a gain-of-functionα8S50P mutation that causes cataracts in mice. When combined with wild-type α8, α8S50P inhibits primary lens fibre elongation; when combined with wild-type α3, it disrupts secondary lens fibre differentiation and elongation. The authors hypothesise that the gain-of-function effects of α8S50P are due to increased channel permeability and fibre-to-fibre transport. The results indicate that gap junctions comprising different connexins regulate lens differentiation in distinct ways, hinting as to why and how different connexin mutations lead to a variety of cataracts.