Receptor for activated C kinase1 (RACK1) was first discovered through interactions between the activated form of protein kinase C, which positively regulates self-renewal and chemoresistance of CD13, and CD133 double-positive HCC cells by directly binding with Nanog. Its binding abrogated the recruitment of E3 ubiquitin ligase FBXW8 and degradation of proteasome to promote stemness and chemoresistance [108]. Here, NANOG is linked to hepatocellular carcinoma.