CPEB2-DT and type 2 diabetes mellitus: Gain- and loss-of-function experiments showed that DRAIR increases anti-inflammatory genes like IL1RN and macrophage differentiation markers like CD36, whereas DRAIR inhibits pro-inflammatory TNF and IL1B, and EC-monocyte binding and phagocytosis, supporting anti-inflammatory functions for DRAIR. Mouse orthologous Drair was also downregulated in T2D db/db mice and its knockdown with locked nucleic acid (LNA) modified GapmeRs in macrophages in vitro and in vivo in non-diabetic mice enhanced Tnf, Il1b, and Il6 genes.