Primary hepatic gastrointestinal stromal tumours (PHGISTs) are rare and frequently misdiagnosed due to their atypical presentation and uncertain origin. The purpose of this article is to present the case of a 79-year-old female patient with a gigantic PHGIST characterized by a predominantly cystic nature—an extremely rare presentation, as most cases of PHGIST are solid. Despite extensive imaging and exploratory laparotomy, the primary origin remained uncertain, leading to questioning about whether it was a true primary hepatic GIST or an atypical metastatic lesion. The initial therapeutic approach involved a surgical procedure aimed to confirm the diagnosis and achieve reductive tumourectomy. Following the surgery, the patient was administered imatinib with a favourable clinical response for four and a half years—an atypical pattern of resistance, as most patients typically develop therapeutic resistance within two to three years. A second surgical intervention was performed to address a cystic lesion localized in the left hepatic lobe, followed by an atypical segment III hepatectomy to achieve macroscopic resection. Subsequently, the patient received sunitinib for two and a half years, which resulted in temporary disease stabilization. However, the sunitinib treatment was associated with hypertension and leukopenia. The patient’s overall survival was 8 years, suggesting that individualized therapeutic strategies and close monitoring might be the key in such cases. Furthermore, this case confirms the role of surgical intervention even in advanced disease stages, with multiple major resections contributing significantly to prolonged survival. The interplay between surgical and oncologic therapies remains essential to guiding clinical decisions. Given the unusual cystic presentation, this case highlights the necessity to expand the pathological and molecular profiling of PHGISTs. Furthermore, the atypical timeline of resistance development and treatment-related toxicity emphasizes the importance of further research into the genetic and pharmacological determinants of PHGISTs. These findings advocate for the refinement of diagnostic, therapeutic, and surveillance protocols tailored to rare GIST subtypes.

Glaucoma progression differs markedly between individuals despite comparable intraocular pressure control, implying additional modifiable contributors to neurodegeneration. We evaluated the joint impact of sleep deficit and inflammatory cytokine trajectories on retinal nerve fiber layer (RNFL) loss. In this 24-month prospective longitudinal observational cohort, 57 participants (19 controls, 19 prostaglandin-treated glaucoma, 19 untreated glaucoma) underwent spectral-domain OCT, validated sleep assessment, and serial IL-6 and TNF-α profiling. Longitudinal models tested independent and interactive effects of sleep deficit and inflammation on RNFL change, and mediation analyses assessed whether inflammation explains the sleep–progression association. RNFL loss rates were −0.20 ± 0.10 μm/year (controls), −1.06 ± 0.89 μm/year (treated), and −1.94 ± 0.78 μm/year (untreated; p < 0.001). Sleep deficit correlated with RNFL loss in glaucoma (r = −0.41, p = 0.010) but not controls, with stronger effects in untreated disease (p = 0.034). Each hour of sleep deficit was associated with 0.09–0.11 μm/year faster RNFL loss (p < 0.05). A combined sleep–inflammation model improved risk stratification (C-statistic = 0.68). Mediation was not supported. Sleep deficit and inflammatory cytokines act as parallel, independent risk factors for glaucoma progression. Integrating sleep and inflammatory profiling may enhance personalized risk assessment beyond pressure-based management.