This trend should be reversed based on the cumulative validated biological knowledge of this system (with regards to the IGF-II/IRA axis role), which is supported by mechanistic explanation and scientific strength, ultimately disclosing the biological differences among IGF ligands and their TK receptors (IRA, IGF1R, and their hybrid variants) in mediating specific and contextual cancer-actionable effects that are now exploitable in the genomic-driven age [9,11,13]. Here, IGF1R is linked to cancer.