In our study published in the early of 2024 by Liu et al., RNase1 has been found to cause an immunosuppressive TME by promoting M2‐like tumor‐associated macrophage (TAM) polarization through its interaction with ALK and activation of the ALK/STAT3 pathway in HCC,[11e] supporting RNase1 functions as an immunosuppressive role in TME. Here, STAT3 is linked to neoplasm.