Previous skin-deep resilience research assessed inflammatory biomarkers such as C-reactive protein,49 but these markers are not necessarily a causal part of mechanistic pathways involving inflammation because they can sometimes be released in response to other signals without underlying injury or infection.50 Thus, to our knowledge, this study provides the first empirical evidence in healthy young people of skin-deep resilience–related alterations to key processes in how immune cells function (eg, how aggressively cells produce cytokines in the face of bacterial challenges). This evidence concerns the gene CRP and infection.