In summary, our current findings demonstrate that HOGA1 functions as a tumour suppressor in ccRCC, which can inhibit the Wnt/β‐catenin–c‐Myc/CyclinD1 axis by regulating the level of HOG (Figure 7), presenting a novel therapeutic strategy focusing on the regulation of hydroxyproline metabolism for ccRCC. This evidence concerns the gene HOGA1 and neoplasm.