In addition, given that the inhibition of CHK1 alone did not lead to complete tumor eradication, despite observed reductions in tumor development, the enhanced infiltration of T cells, and alleviation of T cell exhaustion in vivo, the researchers proceeded to assess the potential of CHK1 inhibition for sensitizing tumors to PD-L1 blocking in immunocompetent RPP mice. The gene discussed is CHEK1; the disease is neoplasm.