Despite HER2, HER3, EphA2 and AXL involving distinct receptor tyrosine kinase (RTK) targets, varying payloads and demonstrating subtle differences in the modulation of the tumour immune microenvironment (TIME), they all clearly show induction of an inflamed, T cell rich TME which facilitated synergy between ADCs and immunotherapy in animal models. The gene discussed is NTRK1; the disease is neoplasm.