Mechanistic evidence also supports the notion that psoriasis-associated systemic inflammation drives this causal relationship: (1) there is overactivation of the interleukin 17/23 canonical pathway central to psoriasis disease pathogenesis, (2) interleukin 17/23 is also found in both the blood and carotid atherosclerotic plaques in people with cardiovascular disease,20,21 and (3) targeted blockade improves imaging-based measures of subclinical CAD in individuals with psoriasis. This evidence concerns the gene IL17A and cardiovascular disorder.