The patient was a 50-year-old man. The patient's father passed away due to tuberculosis and respiratory failure, while his mother remains in good health. The patient has two sisters and a half-brother, all of whom are healthy. At present, the patient does not have any children. He presented with chest tightness, chest and back pain, cough, blood in the sputum, and hypodynamia. The patient had a smoking history of 20 years before developing lung disease. Before the development of the disease, the patient had good health and no reported history of occupational exposure or genetic predisposition within the family. Contrast-enhanced computed tomography (CT) examination of the chest at presentation showed an upper left lung mass shadow (10.7 cm x 8.5 cm x 10.5 cm). The margin was poorly demarcated from the mediastinal pleura comprising multiple flaky low-density necrotic areas. The CT value ranged from 19 to 33 Hu. Whole-body positron emission tomography (PET)-CT scan revealed a mass hypermetabolic lesion in the upper left lung (SUV 8.5) and was considered upper left lung cancer. The lesion was infiltrated along the adjacent bronchial and pleural. And it was intricately related to the aortic arch with peripheral obstructive inflammation. Mild hypermetabolism (SUV 3.0) of left hilar and mediastinal lymph nodes (groups 5 and 6) reflected lymph node metastasis. No metastases were seen elsewhere throughout the body. Blood tumor markers (CEA, NSE, and CYFRA21-1) were normal. Examination of fine-needle aspiration biopsy of the lesion via CT revealed that tumor cells were spindle-shaped or oval, with diffuse infiltrative growth, necrosis of a small number of cartilage components, and loose interstitium. The tumor tissue consisted of both epithelial and mesenchymal tissues, with the epithelial component exhibiting features of low-grade adenocarcinoma. The mesenchymal component, on the other hand, exhibited characteristics of sarcoma with cartilage metaplasia, as illustrated in  Figure 1 . This was consistent with the diagnosis of PB. Immunohistochemistry revealed epithelial components: CK (+), TTF1 (+), CEA (-), CK7 focal (+), CK5/6 focal (+), S-100 focal (+), EMA focal (+); mesenchymal components: Vim (+), S-100 focal (+), Des small (+), CD99 individual (+), CD34 vascular (+), MC (-), Napsin A (-), and Ki-67 (30% +) ( Figure 2 ). Due to the limited tissue sample available, certain immunotherapy predictors, including PD-L1, tumor mutation burden (TMB), and microsatellite stability (MSS), were not evaluated. The diagnosis was classic biphasic PB, and the clinical tumor stage was cT4N2M0 IIIB. The tumor could not be resected because the patient's tumor was closely related to the aortic arch. Therefore, the multiple disciplinary teams (MDTs) believed that radical surgery could be performed. The first-line chemotherapy regimen included paclitaxel 175 mg/m2 (day 1) + cisplatin 25 mg/m2 (day 1-day 3), with a total of four cycles. Chest radiotherapy was given one month after chemotherapy at a dose of 75 Gy/35f, and efficacy was assessed as partial response (PR) after sequential chemoradiotherapy. Follow-up was repeated every three months following the first-line treatment, and PFS was 12.3 months. The patient reported worsening chest pain, with the chest CT showing that the lesion was progressing. The left upper lung lesion was markedly enlarged, and solid changes appeared. The patient experienced difficulty falling asleep due to chest pain, requiring Oxycodone Hydrochloride Controlled-release Tablets at a dosage of 360 mg q12 h to achieve a Numerical Rating Scale (NRS) score below 3. This pain level significantly impacted the patient's ability to work and carry out daily activities. As a distinct subtype of NSCLC, classical biphasic PB (CBPB) poses challenges for second-line chemotherapy alone, and no known driver gene mutation is currently suitable for targeted therapy in this condition. Previous reports have demonstrated that PD-L1 expression was observed in roughly 12% of PPB patients. Furthermore, case studies have identified high PD-L1 expression in patients with CBPB. As such, the combination of chemotherapy and ICIs was considered a potential treatment approach. The treatment was changed to gemcitabine 1250 mg/m2 (d1, 8) and sintilimab 200 mg (d1). After one cycle of treatment, the patient developed third-degree neutropenia, a second-degree rash, and anorexia; we attributed these side effects to gemcitabine. Gemcitabine chemotherapy was discontinued at the patient's insistence, and only sintilimab immunomonotherapy was administered. Over time, the patient's chest pain gradually subsided, and they were able to resume daily activities. The dosage of Oxycodone Hydrochloride Controlled-release Tablets was consequently reduced to 80 mg q12 h. No significant adverse effects were observed during this treatment period. Based on imaging evaluations, the patient's disease state remained stable, classified as stable disease (SD) (see  Figure 3 ). The patient is currently receiving sintilimab for 27 months. His condition was stable, with a performance status (PS) score of 1. The patient has been alive for nearly 40 months and has a good quality of life.