The authors proposed an intriguing model for chronic inflammation-associated HCCs in which myeloid cells represent the source for miR-223 transfer to cancer cells, where miR-223 inhibits HIF-1A expression and indirectly influences the composition of the TME by suppressing the HIF-1A-driven CD39/CD73-adenosine pathway that contributes to PD-1 and PD-L1 upregulation in immune cells. The gene discussed is HIF1A; the disease is cancer.