The application of allelotype microsatellite polymorphisms and X chromosome inactivation analysis in samples from women allow assessment of clonality. Early studies showed that sporadic human pituitary tumors are benign adenomas of monoclonal origin. This implies that they arise from de novo somatic mutation(s) within a single pituitary cell. However, the evidence obtained from a number of studies indicate that morphology cannot predict clonality, clonality within a given tumour may be multiple or single, multiple tumours arising on the background of hyperplasia may be of identical or differing clonality, and multiple "sporadic" tumours within a gland may be of differing clonal origin. Thus, while the early available evidence indicated that pituitary tumours appear largely monoclonal, it is simplistic to assume that this is inevitable and that these cannot be multiclonal in origin. These observations would be entirely compatible with an initiating stimulus resulting in hyperplasia of specific cell types in the pituitary, which itself gives rise to several distinct clones with variable potential to develop into tumours. Such stimuli might include hypothalamic trophic factors, intrapituitary growth factors, or pituitary specific oncogenes.