Since Prelid2 has been demonstrated to be a key downstream effector of MEK/ERK/mTOR-driven liver cancer in response to FBXL6 elevation and KRAS activation, we further evaluated the associations among PRELID2, FBXL6, p-ERK and p-mTOR in 129 paired human HCC and adjacent normal liver tissues from our department. This evidence concerns the gene FBXL6 and liver cancer.