Both Californian and New Zealand kiwifruit industries are based primarily on the same cultivar (Hayward) and have similar problems with regard to gray mold in cold storage. There are, however, major differences in the epidemiology of B. cinerea between the two countries. In California, research evidence collected to date shows that colonization of fruit sepals and receptacles by B. cinerea results in a latent infection of these tissues. As fruit ripen in cold storage, these infections become active and slowly rot the fruit. Therefore, the greater the level of sepal and receptacle infection prior to harvest, the greater the incidence of gray mold in cold storage. Although B. cinerea inoculum from the fruit surface may infect picking wounds during harvest operations, as is the case in the New Zealand system, it is believed that the majority of gray mold decay in storage in California is caused by latent infections of fruit sepals and receptacles. In contrast to the findings in California, studies of the main site of infection (1990 to 1993) and epidemiological studies (1991 to 1995) in New Zealand have concluded that B. cinerea inoculum from necrotic tissues in the canopy collects on the hairy external surfaces of kiwifruit and that this process begins as early as petal fall on developing fruitlets. During harvest operations, B. cinerea inoculum on the fruit surface is transferred to the picking wounds, and if the fruit is in a susceptible physiological state, fruit infection will occur, causing gray mold. Studies of the primary infection site using artificial inoculation procedures found that 91% of the gray mold in cold storage could be directly attributed to the picking wound. Fruit inoculated around the perimeter of the receptacle stem scar exhibited a much lower (5%) incidence of gray mold, suggesting that the majority of the infections are caused by B. cinerea contamination of the picking wound. These findings also suggest that receptacle infections that give rise to gray mold can also occur, but that their incidence is low. Receptacle infections early in the season have been detected in the past, but there was no correlation with gray mold in cold storage. Low levels of latent infections have been detected in New Zealand kiwifruit by other researchers but do not appear to cause the distinctive gray mold symptoms that begin at the stem end of the fruit during cold storage and transit. In conclusion, the main site of infection pathway in California and New Zealand appears to differ, and this emphasizes the need for more research. Tests that identified the picking wound as the main entry point in New Zealand could be repeated in California, and similarly, tests that identified sepals and stem ends as the main entry point in California could be repeated in New Zealand. New research tools, such as fluorescent marker genes, have the potential to be inserted into B. cinerea isolates and could greatly improve our understanding of infection processes and epidemiology of B. cinerea in both California and New Zealand systems.