Interactions between some host factors and the growth and development of Phytophthora infestans, and other pathogens, on and in potato tissue are reviewed. Spore germination and hyphal growth, on or in the surface layers of the host plant, are considered in relation to mechanisms of resistance to penetration. Penetration of living cells of the host, particularly by avirulent races of P. infestans but also by certain non-pathogens, induces a hypersensitive response within the penetrated cell, which involves the accumulation of phenolic compounds such as lignin and terpenoid compounds, e.g. rishitin. Cytological investigations have shown that the walls of hypersensitively reacting cells become resistant to penetration, and that patterns of hyphal growth different from those that occur in penetrated cells of susceptible hosts are established, very soon after penetration. It is considered that these effects become established at too early a stage to be accounted for by the accumulation of the terpenoid compounds. Virulent races of P. infestans appear to be able to inhibit the development of the hypersensitive response, together with the accumulation of certain of the associated compounds. This may be due partly to inhibition of the metabolic pathways involved in the response, and partly to diversion of precursors into pathways leading to the formation of less inhibitory compounds. There is evidence to suggest that a number of pathogens may act in a similar way. Among the compounds which accumulate in response to infection by a number of pathogens is scopolin, which accumulates inside the cell, probably in the vacuole, and a group of conjugates of certain oxygenated cinnamic acids which appear to accumulate within the cell wall. Ferulic acid is a potential precursor for scopolin, the oxygenated cinnamic acid conjugates, and lignin. The possible inter-relationships between the synthesis of these compounds and the mechanisms of resistance and susceptibility are discussed.