Previous studies have indicated that in the hypoxic microenvironment, pancreatic ductal adenocarcinoma (PDAC) cells expressing activated KRAS can upregulate the expression of CA9 by stabilizing HIF‐1α and HIF‐2α, resulting in drug resistance to gemcitabine.[16] To investigate the role of HIF‐2α in RCC, we obtained RNA sequencing (RNA‐Seq) data of RCC tissues and normal renal tissues from the Cancer Genome Atlas (TCGA) dataset and Genotype‐Tissue Expression (GTEx) dataset. Here, HIF1A is linked to pancreatic ductal adenocarcinoma.