As the Ifnar1 surface receptor subunit is necessary to mediate the pleiotropic anti-tumor properties of IFNα (Cheon et al., 2014), we deleted this molecule from CRC cells and from hepatic parenchymal and non-parenchymal cells to identify the mechanism of action (MoA) of continuous IFNα administration in our in vivo system. The gene discussed is IFNA1; the disease is neoplasm.