SMAD3 and neoplasm: Recent studies have reported overexpression of LncDARS‐AS1 in triple‐negative breast cancer (TNBC), where its silencing sensitizes tumor cells to doxorubicin (DOX) by suppressing TGF‐β/Smad3 pathway–induced autophagy, thereby enhancing anti‐tumor efficacy.[13] Additionally, the large‐scale CRISPRi screening of 971 cancer‐related lncRNAs has identified LncDARS‐AS1 as being significantly associated with malignant phenotypes in tumor cells.[11]