As a chronic state of metainflammation is known to be a substantial risk factor in metabolic disorders and cancer [55], [56], [57] and because the absence of CRY in knockout mice has been shown to entail increased expression levels of proinflammatory cytokines including TNF-α and IL-6 [58], we sought to determine if the antimorphic variant potentially could lead to a higher steady-state of inflammation in the transgenic animals. The gene discussed is CRYL1; the disease is cancer.