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Crizotinib is the first-line drug for non-small cell lung cancer (NSCLC) patients who display anaplastic lymphoma kinase (ALK) rearrangement. With 60% overall response rate, crizotinib significantly prolongs median progression-free survival (ranged 8-10 months) of ALK rearrangement NSCLC patients.However, there are some adverse events from crizotinib, including diarrhea, weakness and nausea. Here, we describe a 47 years old woman with ALK-rearranged NSCLC who developed interstitial pneumonia (IP) induced by crizotinib. A female patient was diagnosed as the left lower lobe adenocarcinoma stage IV (T4N2M1, pleural metastasis) via lung biopsy and was detected wild-type EGFR and 18% ALK gene rearrangement from paraffin section. However, after going through 7 cycles of chemotherapy, she rejected chemotherapy because side effect and still experienced progression of the disease. Subsequently, crizotinib was prescribed as a targeted therapy. After 32 days, visible reduction in size was observed on the pulmonary mass and metastases found in brain and liver, but the patient presented drug-induced level 4 interstitial pneumonia. In a nutshell, the curative effect of crizotinib is worthy of note, but clinicians should also weigh the advantages and disadvantages, prior its usage.

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Objective This study aims to explore the correlation between ferroptosis and immune microenvironment (IME) in diabetic kidney disease (DKD) to provide a new clue for exploring the underlying molecular mechanisms. Methods Corresponding RNA data of DKD patients were downloaded from GEO databases. The weighted gene co-expression network analysis (WGCNA) was used to construct the network, and the selected hub genes, then, overlapped with ferroptosis-related genes (FRGs) from FerrDb. Consensus clustering was performed to identify new molecular subgroups. ESTIMATE, TIMER and ssGSEA analyses were applied to determinate the IME and immune status. Functional analyses including GO, KEGG and GSEA were conducted to elucidate the underlying mechanisms. Results Two molecular subtypes were identified based on the expression of FRGs. ESTIMATE algorithm revealed that there were significant differences in ESTIMATE score between these two clusters of DKD patients, with no significant difference found in stromal score and immune score. In addition, TIMER algorithm indicated there was a significant difference in the degree of T cell infiltration. The ssGSEA algorithm showed immunity was mainly concentrated in thick ascending limb and distal convoluted tubule in adult kidney. GO, KEGG and GSEA analyses revealed that the differentially expressed genes (DEGs) were mainly enriched in immune and metabolism associated pathways. Conclusion The ferroptosis may be induced by dysregulation of IME, thereby accelerating the progression of DKD. Our work could be applied to provide a new clue for exploring the underlying molecular mechanisms and sheds novel light on the therapy strategy of DKD.