discovered that localized mechanical crosstalk contributed to define the secretory events in the immune synapse.[33] While the pulling forces of LFA‐1 were pivotal in secretory domains of the immune synapse, the depletion of talin disrupted such forces thus impacting the release of perforin and lytic enzymes from T cells, impairing the cytotoxicity of T cells against pathogens and tumor cells. The gene discussed is PRF1; the disease is neoplasm.