A 45-year-old female presented with complaints of progressively increasing dysphagia mainly to solids for last four months associated with significant loss of weight and appetite. She denied any history of heartburn, regurgitation, caustic ingestion, trauma, fever, cough, hemoptysis, change in voice, difficulty in breathing, hematemesis, or melena. On examination, her vitals were stable, mild pallor was present, and there was no lymphadenopathy. Her respiratory and gastrointestinal examination was within normal limits. On routine investigation, the hemoglobin level was 9.1 gm%, the total cell count was 8800/cumm, the platelet count was 180,000/cumm, the serum creatinine level was 1 mg/dL, the aspartate transaminase level was 40 IU/mL, and the alanine transaminase level was 38 IU/mL. Her barium swallow showed a smooth indentation of distal esophagus along the right lateral aspect with significant luminal compromise. Upper gastrointestinal endoscopy was suggestive of a smooth stricture with normal overlying mucosa seen in the lower esophagus starting at 28 cm from the central incisor (Fig. 1A). The scope could not be negotiated beyond. Subsequently, a contrast-enhanced computed tomography (CT) of thorax revealed a heterogeneously enhancing mass lesion at the lower one-third of the esophagus causing near-complete lumen occlusion (Fig. 1B and C). In order to characterize the lesion and enable biopsy, esophageal dilatation was done using the Savory-Gillard dilator. Subsequently, the visualized esophageal mucosa at the stricture site was normal, and a repeat mucosal biopsy was negative for malignancy. Then, an EUS was done revealing a 3.3 cm x 2.5 cm heteroechoic mass lesion in the submucosal region of the distal thoracic esophagus, which was in close proximity to the left atrium (Fig. 2A). EUS-guided FNA of the mass showed a cellular smear with clusters of atypical cells with nuclear polymorphism, scant cytoplasm, coarse chromatin, and small nucleoli suggestive of squamous cell carcinoma (SCC) (Fig. 2B and C). This was confirmed on immunohistochemistry, which was positive for cytokeratin 5/6 and p53. The serum carcinoembryonic antigen level was 18 ng/mL. To rule out a metastatic disease, a whole body 18-flourodeoxy glucose-positron emission tomography (PET) scan was done, which showed an avid uptake in the esophagus in the region of the mass and in the pelvis, suggestive of bone metastasis (Fig. 3A and B). ENT examination and bronchoscopy were normal. A final diagnosis of primary esophageal intramural SCC with bone metastasis was made. The patient is currently on palliative chemoradiotherapy. She was given capecitabine and oxaloplatin-based chemotherapy together with external beam radiotherapy to achieve a durable response to relieve the malignant dysphagia as repeated settings of endoscopic dilatation had only short-lived response. The patient was non-affording for self-expandable metal stenting, and brachytherapy was technically difficult. At present, on two months of follow-up, her dysphagia has partially relieved. Bone pain is controlled with opioids. There is no change in the size of the original tumor on imaging.