Upon hepatocyte-dictated E-cadherin upregulation in prostate cancer cells and cell-cell adhesion through homeotypic binding, prostate cancer cells reactivated canonical survival pathways, such as PI3K/Akt, MEK/ERK, and JAK/STAT in response to chemotherapy and/or death signals, gaining resistance to treatment in a proliferation-independent manner [46,47] (Figure 1). The gene discussed is SOAT1; the disease is prostate cancer.