But at face value this looks very promising.
This identifies one way solid tumors avoid immune attack and identifies corresponding therapeutic targets that could span solid tumor types.
EPO (erythropoietin) (aside from stimulating red-blood-cell production) also converts tumor-local macrophages from attacking to suppressing immune attacks. Tumors are shown to produce EPO themselves.
Tumors spontaneously regressed due to revived immune response when blocking either EPO or the EPO receptor on the macrophages.
The model was murine liver cancer, but high blood EPO levels are known to be poor prognosticators in many solid tumor cancers.
This summary points to NRF2 (nuclear factor erythroid 2-related factor 2) as a regulatory target, but without any detail.
AFAICT there are no approved drugs blocking EPO receptors and no drugs to reduce EPO; there are some anti-anemia drugs that increase production.