Once the inoculum of B. cinerea comes into contact with the host and starts to be active in the phyllosphere of a susceptible host tissue, a series of events take place. These events may develop into a process that leads to necrosis of the host, or may end in an arrested infection with minimal damage to the host tissue. Increased susceptibility to the pathogen is associated with factors that enhance ageing of the host tissues, such as the plant hormones ethylene and abscisic acid and elevation of free radical levels in the host tissue. Decreased susceptibility is obtained by inhibiting the production or activity of such factors in the presence of increased levels of plant hormones such as gibberellic acid, and by increasing the calcium content of the cell walls and by scavenging of free radicals in the host tissue. There is evidence for the induction of resistance in hosts affected by B. cinerea. Host tissues challenged by B. cinerea react at the DNA, RNA and protein level and accumulate pathogenicity related proteins, phytoalexins or other phenolic compounds. Deposition of polymers in cell walls and lignification have also been recorded in various hosts. The role of each of these factors in relation to protection is not clear. Moreover, some of the phenomena may occur too late to protect the host tissue against infection. Although the inhibition of specific proteins such as polygalacturonases has been suggested as a mechanism by which to inhibit disease, it is unlikely that the inhibition of one enzyme, would lead to significant restriction of infection. However, simultaneous inhibition of several hydrolytic enzymes produced by the pathogen should result in disease suppression. Possibilities of reducing the susceptibility of hosts or arresting further development of localized infections are discussed.