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Y. Mérot †, MD, Department of Dermatology, Centre Hospitalier Universitaire Vaudois, CH–1011 Lausanne (Switzerland) Although Merkel cell (MC) was described more than a century ago by Merkel [1], the involvement of MC within a pathologic process remains unclear. Besides the so-called MC carcinoma (neuroendocrine carcinoma of the skin) ‚ hyperplasia of MC has been observed. Gould et al. [2, 3] reported the existence of such a feature within chronically damaged actinic skin. Hyperplastic MC were distributed as basal rows and showed focal and architectural abnormalities [3]. Less frequently, these cells were observed isolated or in clusters within the stratum spi-nosum. We recently expanded these observations to actinic keratoses [4] of which only the hypertrophic varieties demonstrated hyperplasia of MC. Furthermore, this hyperplasia was almost restricted to those lesions with club-like epidermal proliferations. Because similar clublike proliferations where MC cluster are normal morphological patterns of some epithelia, e.g. the parakeratotic zone of the rabbit lip epithelium or the ingrowing hair follicles of the mouse skin during embryogenesis, and because such MC were also pointed out within involved skin of psoriasis [5] ‚ a situation where club-like proliferations are common, we proposed that the MC hyperplasia could result as a consequence of a specific differentiation of the epithelia. In this issue (p. 73), Wollina rises the question wether MC hyperplasia or epidermal hyperplasia triggers the other, and refers to an important study conducted by Jones and Munger [6] in opossum. Sequential events occurring in this experiment can be summarized as follows: (i) partial neuralectomy; (ii) compensatory hyperplasia of the dorsal root ganglia with an increased innervation of both the dermis and the epidermis; (iii) epidermal hyperplasia, and (iv) precocious hair development. This experiment suggests to Wollina that MC hyperplasia is a prerequisite to the epidermal hyperplasia rather than a consequence. This could imply that the preexisting intraepidermal MC attract and guide the nerve endings to their final location. This would be in accordance with the hypothesis of MC target for the ingrowing nerves [7]. Unfortunately, Jones and Munger [6] did not look for MC hyperplasia during the course of epidermal changes in the skin they studied. However, there is some evidence favoring the opposite. The sequence of events of hair development during mouse skin embryogenesis clearly shows that a follicle-like structure precedes the appearance of follicular MC [Mérot, Y.: unpubl. data]. MC are only recognisable at the 12th day of the gestation [8] when the hair follicle enters stage 2 or 3 of its development according to Davidson and Hardy’s [9] classification. At that time, there is no connection between MC and the ingrowing nerve endings [10]. At least in this physiological condition, epithelial changes precede MC. But MC could still function as a target for ingrowing nerves.