Modulating the recruitment of proximal signaling molecules, such as NCK and LCK, with novel small molecules could refine the activity of endogenous TCRs in autoimmune diseases and immunopathologies or improve the function of engineered receptors in cancer therapy, while overcoming off-target effects of classical kinase inhibitors, targeting conserved enzymatic activity rather than a specific protein-protein interaction. The gene discussed is NCK1; the disease is autoimmune disease.