A recent report also revealed that both Arid1a and PIK3CA mutations may cooperatively promote tumour development through the sustained IL-6 overproduction in ovary cancer, indicated by a mouse model [24, 25], where Arid1a protects against the inflammation-driven tumorigenesis, which is similar to our found in the Arid1a deficiency-driven HCC. This evidence concerns the gene PIK3CA and neoplasm.