As reported by Jaime-Perez et al., recent molecular theories explaining the pathophysiology of Evans syndrome include deficiencies in cytotoxic T-lymphocyte-associated antigen 4, lipopolysaccharide (LPS) response beige-like anchor protein, tripeptidyl peptidase two, and a decrease in the cluster of differentiation (CD)4/CD8 ratio [2]. The gene discussed is CD8A; the disease is Evans syndrome.