## 1 Introduction  
Similar to other cutaneous lesions with malignant transformation potential, keratoacanthoma represents one of the pathologies with a negative impact on public health systems; a significant increase in the number of cases diagnosed is being reported worldwide. It is described and classified by [PERSON] et al. as a premalignant precursor lesion of squamous cell carcinoma of the skin, one of the most aggressive oncological pathologies developed in epithelial tissues. At the same time, the latest studies also support the idea that keratoacanthoma is a type of carcinoma in situ. Although some meta-analyses of the last decade indicate an average of about 12%, data on the risk rate of malignant transformation are contradictory and incompletely elucidated [1, 2, 3, 4].  
The non-specific symptomatology of these lesion types negatively influences referral to specialist clinics making it impossible to accurately and completely quantify the risk of malignancy in the early stages of progression. In addition, clinical studies reveal the phenotypic and morphological variability of these lesions, a variability conditioned and determined by the action of highly heterogeneous etiopathogenic mechanisms [5, 6, 7].  
The identification and description of the cellular and molecular characteristics of keratoacanthomatous lesions facilitates the understanding of pathogenic mechanisms specific to the early stages of epidermal carcinogenesis [2, 7, 8].  
Over the years, in the case of keratoacanthoma (molluscum sebaceum) the histopathological examination, considered the \"gold-standard\" in establishing the diagnosis, describesseveral aspects, depending on its evolution. Thus, at onset, a marked proliferation of the epidermis, acanthosis, dyskeratotic cells, with a reduced degree of keratinisation and inflammatory infiltrate in the dermis underlying the lesion are revealed. During the stability period, a differential diagnosis between keratoacanthoma and well-differentiated squamous cell carcinoma remains difficult [3,6,9].  
Photon microscopy, the resolution power of which is limited, does not always reveal features suggestive of epithelial lesions with mild-to-moderate dysplasia. Thus, there may be cases in which carcinomas develop on dysplastic lesions undiagnosed or unidentified in previous biopsies [4,6,10].  
Epithelial-mesenchymal transition (EMT) is a key time process in malignant transformation. At this stage, epithelial cells acquire morphological characteristics of fibroblasts through a process regulated by dermal-epidermal interactions. These interactions condition cell growth and differentiation in the epidermis. As early as 1981, [PERSON] et al. observed that during premalignant hyperplasia, defined as epidermal hyperplasia progressing to carcinoma, basal layer keratinocytes maintain their normal architecture, with disorganization of intercellular coupling structures and enlargement of intercellular spaces [9,10,11,12].  
Starting from all the aspects mentioned above, the present study aims to evaluate the evolutionary potential of keratoacanthoma lesions by describing the tissue microenvironment at the ultrastructural level, revealing the cellular interactions involved in the staging and efficiency of diagnostic and therapeutic protocols.