Current treatments for advanced TFE3‐RCC, such as tyrosine kinase inhibitors, mTOR inhibitors, and immune checkpoint inhibitors, are not consistently effective in all patients.[2, 15, 16, 17, 18] This may be because TFE3‐RCC is considered an “immunologically cold tumor,” and not all cases involve EGFR or mTOR activation.[30] SV2B is highly expressed in TFE3‐RCC and can promote its progression via the NF‐κB pathway. This evidence concerns the gene SV2B and neoplasm.