Based on our observation that Igf2bp1 genetic inhibition in tumor cells increases expression of pro-inflammatory genes, increases sensitivity of melanoma cells to interferons stimulation, induces stimulation of intracellular Ifn-γ production in tumor-specific mouse T lymphocytes, and increases accumulation of immune cells in the tumor site, we performed in vivo modeling of anti-PD1 immunotherapy using SM1 mouse melanoma cells with CRISPR/Cas9 control and Igf2bp1-KO in syngeneic C57BL/6 mice. Here, IGF2BP1 is linked to neoplasm.