As overexpression of tumor-associated antigens (TAA), ENO1 and FUBP1, may break self-tolerance, inducing an immune response against them [35, 36], the presence of circulating aAb to ENO1 and FUBP1 was analyzed in sera from the two cohorts of PDA patients (Table 1). The gene discussed is FUBP1; the disease is Patent ductus arteriosus.