Reciprocally, inflammatory cytokines present in the microenvironmental milieu, such as IL1β, IL6, and TNFα, upregulate PDA cell expression of ST3GAL3-4, FUT1-2, and FUT6, resulting in increased sLex, SLey, and α2,6-sialic acid levels, suggesting that glycosylation of PDA cells is modulated by inflammatory microenvironments (Bassagañas et al., 2015; Fig. 3). Here, IL1B is linked to Patent ductus arteriosus.