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Genitogluteal porokeratosis (GGP) encompasses a spectrum of keratinization disorders affecting the genital and gluteal regions [1]. While distinct entities like Porokeratosis Ptychotropica (PP) and Penoscrotal Porokeratosis (PSP) are defined by multiple lesions and specific histology (multiple cornoid lamellae; MCL), we report a unique case of a solitary scrotal plaque in an elderly man. This case clinically mimics Porokeratosis of Mibelli (PM) but histologically exhibits the MCL characteristic of PSP/PP, suggesting that mechanical stress may modify the expression of clonal porokeratosis. An 82-year-old man presented with a solitary, asymptomatic, 20-mm erythematous plaque with a raised keratotic border on the scrotum, persisting for 1 year. There were no satellite lesions or involvement of the buttocks. The clinical impression included Bowen's disease or psoriasis. However, histopathological examination revealed MCL distributed throughout the lesion, accompanied by hypogranulosis and dyskeratotic cells. Immunohistochemistry showed p53-positive cells beneath the cornoid lamellae and focal p16 expression, ruling out malignancy (Figure 1). The postoperative course was uneventful, and no recurrence was observed at the 2-month follow-up. This case presents a diagnostic paradox. Clinically, the solitary nature and the patient's advanced age favor a diagnosis of PM, as PSP typically presents as multiple lesions in young men (20s–30s) [2]. However, the histological finding of MCL is traditionally considered pathognomonic for PSP or PP and is rarely seen in classic PM, which typically features a single peripheral cornoid lamella. We propose that this case represents a “Solitary GGP with MCL,” bridging the gap between PM and PSP. Recent breakthroughs by Kubo et al. have established that porokeratosis results from the clonal expansion of keratinocytes with mevalonate pathway defects acquired via a “two-hit” mechanism (germline and somatic mutations) [3]. Furthermore, Saito and Kubo recently identified that FDFT1 gene-specific epigenetic silencing underlies non-hereditary, localized forms of porokeratosis [4]. This epigenetic mechanism may explain the sporadic, solitary presentation in our elderly patient. While the lesion likely originates from a single clone (consistent with PM), the penoscrotal anatomy introduces unique environmental factors—specifically, chronic friction and rugose skin folds. We hypothesize that mechanical stress in this region disrupts the centrifugal expansion of the clone, causing the fragmentation of the cornoid lamella into the “multiple” stacks seen in PSP and PP. However, other mechanisms should also be considered. Minami-Hori et al. reported that cornoid lamellae are frequently associated with follicular infundibula and acrosyringia, suggesting that anatomical adnexal structures contribute to MCL formation [5]. Thus, MCL formation might occur not only as a result of multicentric clonal expansion (polyclonality) but also potentially as a reactive phenomenon in a single clone exposed to local environmental stress or anatomical factors. In conclusion, solitary GGP in the elderly can present with MCL. Our findings suggest that site-specific factors, such as friction or adnexal structures, might influence the histological architecture of porokeratosis. The presence of MCL should not automatically exclude a diagnosis of solitary variants like PM, although further accumulation of cases is needed to clarify the pathogenesis. The authors have nothing to report. The authors have nothing to report. We obtained written informed consent from the patient to publish his clinical details. The authors declare no conflicts of interest. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.