Another study suggests that in intrahepatic cholangiocarcinoma (ICC), nucleolin (NCL) undergoes Kla modification, which inhibits the alternative splicing of the precursor mRNA of MADD, thereby increasing its integrity and stability, upregulating mitogen-activated protein kinase-activated protein kinase (MADD) and activating the mitogen-activated protein kinase (MAPK) signaling pathway, facilitating ICC growth [167]. This evidence concerns the gene KL and intrahepatic cholangiocarcinoma.