Hong et al. found that T-cell leukemia 1 (Tcl1) could interact with heterogenous nuclear ribonucleoprotein (hnRPK) and enhance G6PD pre-mRNA splicing, thereby increasing G6PD expression and, subsequently, the progression of HCC; however, this regulation could be canceled by the inactivation of Tcl1 through phosphorylation by phosphatase and tensin homolog (PTEN)-induced glycogen synthase kinase-3β (GSK3β) [86]. The gene discussed is G6PD; the disease is hepatocellular carcinoma.