RUNX1 and cancer: A possible reason might be that this polymorphism (T to C) was a polymorphism in the fourth intron of PDCD1,[24] the substitution of T for C in the enhancer within the intron might disrupt the binding site of RUNX1, alter the regulation of gene expression, and influence the PD-1 pathway.[24] PDCD-1.3 (rs11568821) polymorphism may impair the inhibitory effect of PD-1 and thus may lead to positive regulation of cytotoxic lymphocyte activity in T allele carriers.[5,24] Thus, variant TC genotype might contribute to decrease risk of cancer.