Although the bispecific C-7 VHH could also potentially trigger the activity of CD16+ non-NK cells, such as non-classical/intermediate monocytes that constituted the second-largest CD16+ immune cell subset in metastatic CRC patient PBMC, we found that the dominant antitumor effect was mediated via the activation of CD16+ NK cells as depletion of non-classical/intermediate monocytes did not affect the tumor growth control triggered by C-7. The gene discussed is FCGR3A; the disease is neoplasm.