“…5,8 However, this explicative model is hardly applicable in those cases in which the tum or arises in lesions of DLE in a sun-protected area.9 Genetic predis position, severity of DLE, and human papillomavirus infection of discoid lesions are other hypothesized secondary factors. 4,8,9 Furthermore, some authors have also speculated on a hypothetical, but indeterminate, contribution of the chronic scarring process.8 This, together with chronic inflammation per se, has also been considered a possible causal factor for the development of soft tissue sarcomas from DLE, by unknown mechanisms. 6 In general, scars of various origin are common vulnerable areas for the subsequent development of cutaneous tumors, including AFX, 10,11 and according to recent studies, such an event would be due to the interruption of the normal innervation and lymphatic network occurring in scarring sites, with a consequent imbalance of lymphatic circulation and release of neuromediators.…”