Cerebral venous thrombosis (CVT) is a rare type of cerebrovascular event in which the thrombosis occurs in a vein of the cerebral venous system. The diagnosis could be challenging due to the great clinical variability, but the outcome is favourable in most cases, especially in the case of early diagnosis. Anticoagulant therapy is the core of CVT management and currently consists of heparin in the acute phase followed by vitamin K antagonists (VKAs) in the long term. The ideal duration of anticoagulant therapy is still unclear, and the same criteria for the treatment of extracerebral venous thromboembolism currently apply. In this paper, we reviewed the literature regarding the use of direct oral anticoagulants (DOACs) in CVT since in recent years a considerable number of studies have been published on the use of these drugs in this specific setting. DOACs have already been shown to be equally effective with VKAs in the treatment of venous thromboembolism. In addition to efficacy, DOACs appear to have the same safety profile, being, on the other hand, more manageable, as they do not require close monitoring with continuous personalised dose adjustments. In addition, a further advantage of DOACs over VKAs is the possibility of anticoagulant prophylaxis using a reduced dosage of the drug. In conclusion, although the use of DOACs appears from preliminary studies to be effective and safe in the treatment of CVT, additional studies are needed to include these drugs in the treatment of CVT.

The FLT3-ITD mutation is a critical prognostic marker in acute myeloid leukemia (AML) and recent clinical trials demonstrate that FLT3-based measurable residual disease (MRD) is both prognostic and predictive, guiding therapeutic interventions in intensive and post-transplant settings. Conventional detection methods lack the sensitivity required for effective MRD monitoring. We developed a patient-specific droplet digital PCR (ddPCR) approach achieving analytical sensitivity of 10⁻⁵ (0.001%) for FLT3-ITD quantification. In our cohort, ddPCR enabled longitudinal monitoring of clonal dynamics, allowing the detection of re-emerging FLT3-ITD clones months before hematologic relapse and earlier than standard capillary electrophoresis. Notably, 25% of patients who relapsed as FLT3-ITD positive despite being classified as FLT3-negative at diagnosis harbored detectable microclones when retrospectively analyzed by ddPCR, suggesting that FLT3-ITD-positive relapse frequently originates from pre-existing subclones below conventional detection thresholds. These findings challenge current diagnostic classification and may influence risk stratification and treatment decisions, particularly regarding FLT3 inhibitor eligibility. While ddPCR is limited to tracking known dominant clones, it represents a practical, cost-effective solution for high-sensitivity MRD surveillance. In the era of targeted FLT3 therapies, integrating sensitive molecular monitoring into routine AML management may enable timely therapeutic adjustments and improve patient outcomes.