The most significant finding of the past year in gap junction research
has been the association of connexin defects with human diseases. Con
nexin32 mutations cause X-linked Charcot-Marie-Tooth disease, a demyel
inating peripheral neuropathy. Mutations in connexin43 may underlie ca
rdiac malformations in visceroatrial heterotaxia syndromes. Genetic ap
proaches and gene targeting have provided new insights, but also raise
new questions concerning connexin function, the significance of conne
xin diversity and the regulation of intercellular communication.