The histogenesis of precancerous lesions and of carcinoma in situ has undergone deep changes over the past ten years. In particular, concepts of re-epidermisation by indirect metaplasia has made it possible to understand the progressive process which results what are generally described as dysplasias. These lesions were previously considered as being made up of two groups : regular dysplasia with slight or moderate dyskaryosis, with a good prognosis, and irregular dysplasia with severe dyskaryosis; but they are now felt to be non-obligatory stages in the same process which may stop for a time, regress or on the contrary accelerate and become an invasive carcinoma. There is no clearly defined limit between dysplasias and carcinoma in situ. These concepts are confirmed by cytology, histology and other methods (histophotometry, cytogenesis, biochemistry, etc). The aetiology of these lesions is involved with the hormonal environment and vaginal pH which would appear to play a role in the epidermoid differentiation of undifferentiated or reserve cells which are the basis of the constitution of preneoplastic lesions. The penetration of mutagens into these cells is explained by the hypothesis of amoeboid movements of undifferentiated cells which bring the nuclear heterochromatin into contact with the external surroundings where carcinogenic histones are found.