The first evidence that the loss of HPK1 has a positive impact on T cell response to cancer in vivo came when Alzabin et al. demonstrated in the Lewis lung carcinoma model that adoptive transfer of HPK1-/- T cells is sufficient to confer host mice with the ability to reject the 3LL lung carcinoma, revealing the importance of HPK1 in the control of the T cell intrinsic response to cancer antigens (Alzabin et al., 2010). The gene discussed is MAP4K1; the disease is cancer.