This revealed that besides one NKp30-targeting paratope that was unfunctional in combination with both EGFR-directed antigen binding sites (similar to an EGFR-targeting Fc-silenced negative control), 12 out of 13 NKp30-directed binders triggered tumor cell lysis in conjunction with both EGFR-paratopes to some extent (Figure 4A). The gene discussed is EGFR; the disease is neoplasm.