Given the absence of CCR7 on effector memory circulating T cells (Farber, Yudanin, & Restifo, 2014), these cells could traffic back to secondary lymphoid organs employing alternative mechanisms like through CXCR3/CXCR3L interactions (Ferrando‐Martinez et al., 2018; Khan et al., 2000), a mechanism presumably dependent on local tissue infection and inflammation. This evidence concerns the gene CXCR3 and infection.