Dear Sir,We thank the authors for taking great interest in our paper and their comments.[1] However, considering the etiological heterogeneity in our case series with a varied spectrum of uveitic patients, any attempt to generalize the association of central serous chorioretinopathy (CSC) may not be straightforward. For example, it will be difficult to calculate the cumulative dose of steroids in our patients—as 6 of our 26 patients were using topical steroids, and 2 developed CSC following periocular steroid injections.[2] Moreover, the development of CSC is not always dose-dependent. Further, corticosteroid, in any form, is usually avoided in patients with a history of CSC and none of our patients had a history of CSC. All of the patients in our case series had varying degrees of inflammation at the time of diagnosis, and the subsequent management of these cases has already been described in the paper.[2] It is always challenging to manage a case of uveitis in the presence of CSC as many a time the cause of decrease in vision is interpreted as worsening of the primary inflammation. Two of our six patients with CSC who presented with bullous retinal detachment were started on high-dose corticosteroids, elsewhere misinterpreting them as worsening of Vogt-Koyanagi-Harada disease (VKH). It is of utmost importance to differentiate between the two entities as the modalities of treatment are quite opposite; while steroids help resolve inflammation in VKH, they are contraindicated in CSC. A combination of ophthalmoscopic and angiographic findings is usually helpful to clinch the correct diagnosis in such scenario. VKH syndrome, sympathetic ophthalmia, and posterior scleritis have a similar angiographic characteristic; the multiple pinpoint hyperfluorescence in early frames show placoid pooling in late frames whereas the leaks in CSC increases in size and intensity. In addition, the lack of optic disc staining in CSC is an important feature.[3] Indocyanine green angiography may rescue the clinician in differentiating such scenarios. Furthermore, optical coherence tomography examination in VKH can show subretinal septa with a multilobular exudative retinal detachment and undulating folds of the retinal pigment epithelium and Bruch membrane. The clinical sign like a “dark spot” and multiple pigment epithelial detachment (PED) seen on imaging can help differentiate the two.[4] PED is uncommon in inflammatory conditions. However, the absence of PED does not rule out CSC as non-PED CSC is more common especially in the acute state of first attack. We agree that in the presence of ocular inflammation, signs of CSC might be overlooked. This, precisely, was among the primary purposes of describing the case series highlighting the management difficulties of such situations. The diagnosis of such cases require a high index of suspicion and appropriate interpretation of ancillary investigations.