Our studies indicate that the induction of LCK is necessary for the increased antigen‐induced CAR T‐cell activation, IL‐2/IL‐15 receptor subunit (CD25, CD122 and CD132) expression and cytotoxicity of PTPN2‐deficient CAR T cells, whereas the concomitant direct promotion of STAT5 phosphorylation and cytokine signalling might not only facilitate the acquisition of CTL activity, but also promote homing to CXCL9/10/11‐expressing tumours through the induction of CXCR3. The gene discussed is LCK; the disease is neoplasm.