Thank you for the additional discussion of this case (I think it was 6th July which was a regressing KA). I could spend a very long time discussing KA v's SCC.Firstly a serious caveat - I am not sure the diagnosis is safe in the hands of experts let alone non-experts to be honest!That said we in Warwick are (currently) firmly in the camp that KA is a distinct Clinical-Pathological diagnosis.Provided a lesion is typical clinically and histologically we can make a confident diagnosis (in the knowledge that there is a risk of true malignant transformation and exceedingly rarely metastasis - in otherwise typical - but usually to local lymph nodes). Early KA (in our view) does often include quite striking cellular pleorphism and typically the early lesions have highly proliferative infiltrative (not pushing circumscript borders like well differentiated SCC) borders with prominent elastic incorporation in the proliferative phase. Despite the frighteningly worrying peripheral component in all areas of the tumor there is central (often abprupt) transition to highly differentiated and distincitive pilar keratinisation. In excision biopsies the symmetrical exoendophytic nature and rounded silhouette are obviously helpful. In a small biopsy one can easily diagnose an early KA as a poorly (not well) differentiated SCC if one does not spot the central differentiation in all islands (suggest multiple levels are examined on small biopsies to demonstrate this feature of KA). Incorporation of elastic can be a feature of poorly differentiated SCC but not, in my experience, a well differentiated SCC (that usually have much more pushing mitotically inactive borders)and in my view is rarely a true diagnostic consideration in the histological differential diagnosis of an early KA. Obviously clinical information is essential as well differented SCC does not grow rapidly in a few weeks like a KA. Otherwise typical clinicopathological KA with frank (bowenoid) atypia (probably about 30% of our cases of early KA!) in my opinion is of uncertain biological significance but would lead us to recommend complete excision (in partial biopsies i.e. malignant transformation must be a serious consideration)and probably follow-up as for SCC (when seen in isolation in an excision specimen). We tend to opt for complete excision with clear margins on most cases (of even classicaly clinicopathological early KA) in any case. Often patients prefer not to have an unsightly smelly rapidly growing lesion on their face and conservative excision is cosmetically acceptable in good hands. However for some typical (biopsy confirmed) cases watchful waiting (i.e. active close follow-up with a low threshold for excision of persistent or actively growing lesions) may be an option for some individual lesions for some patients. Obviously patient's and clinicians will vary on how brave they are prepared to be watching a lesion that may or may not undergo true malginant transformation. Because of the complexity of the above and the many caveats you will hopefully understand why I am saying I am not sure the diagnosis of KA is entirely safe! I have not even discussed the many lesions we are now referring to as follicularSCC that may closely, at first glance, resemble KA (often they have acantholysis and central follicular mucin - features we do not see in KA - but most are well differentiate with lobular circumscribed pushing bordres). We also often sit on the fence or admit defeat in a significant proportion of cases (even with good clinico-pathological corration). We certainly discuss each and every case in a multi-disciplinary setting and I hope an awareness of the difficulties and a shared team approach is the safest way of managing these patient's