To the Editor: We would like to thank Dr Su et al1 for sharing their insights on dural arteriovenous fistulas (DAVFs) and thoughtful and duly comments on our recent article “Angioarchitectural analysis of arteriovenous shunts in dural arteriovenous fistulas and its clinical implications.”2 Based on the histopathological studies and their experience of DAVFs, Dr Su et al point out that fistulas are not formed directly at the dural sinuses but between the dural artery and the dural vein (in the dural sinus wall) before draining into the sinus or the bridging vein.1,3,4 We agree with these classic histopathological finding; however, the main focus of our study was to describe and discriminate the “angiographic” shunt patterns in light of the connections between the shunt, the sinus, and the cortical veins to unveil their practical implications. In this regard, there were specific patients in whom the targetable fistulous channel—regarding the branching patterns and the caliber changes of the vessels—could not be identified but showed functionally direct connections with the sinus. The histopathological basis for these kinds of shunt remains speculative. The variations in the anatomy of the dural vessels (length, location, etc), secondary changes associated with venous hypertension, thrombosis, inflammation, angiogenesis, and dural wall alterations alongside the temporal changes may have manifested as this pattern.3-8 Interestingly in our series, multiple shunt types were noted in several patients (n = 7), more frequently as the coexistence of the direct sinus fistulae and mural channel-type shunts (n = 5), suggesting the dynamic nature of this disease. Extensive histopathological studies are crucial to shed light on these compelling questions but are extremely limited. Meanwhile, angiographic discrimination of the different characteristics of the shunts, such as the diffuse direct connections or channel-like structures or bridging vein type shunts, and their connection patterns with the sinus and the cortical vein are paramount for effectively targeting the lesion and predicting the behavior of the liquid embolic agents. The presence of pial arterial supply to the DAVF has gained much interest. There are concerns that these patients may be associated with postprocedural rupture of the fragile neovascularized vessels after venous outflow obstruction and inadvertent reflux of the embolic agent into the pial arteries.9,10 The presence of the pial feeders are known to be strongly associated with the tentorial DAVFs.9,10 Our series included only the superior sagittal and transverse sigmoid sinus DAVFs; thus, analyzing the implications of pial supplies was considered beyond the scope of our study. However, this is an interesting topic that deserves further scrutinization. We greatly appreciate the comments and insights by Dr Su et al. DAVFs are fascinating but also complex and challenging diseases. We wish for further technological progress and the power of collective intelligence in understanding and overcoming this intriguing disease.