Here and as a result of linking the reported results and our predicted correlations, the model is partially proposing the crosstalk of all these pathways to enhance the hepatic cancer stemness in means of: 1- MYC and STAT3 may connect JAK/STAT, Wnt and PI3K in HCSC to activate expression of CD44 stemness marker, mTOR as a self-renewal and drug resistance inducer and inhibit apoptosis via activation of Bcl2. The gene discussed is MTOR; the disease is liver cancer.