RAB26 and acute respiratory distress syndrome: Previous studies have shown that Rab26 inactivation induces the mistrafficking of GPCRs, which leads to receptor dysfunction that is directly linked to cell function disorders; other studies have shown that treatment with Rab26 siRNA destroys barrier function and that Rab26 even promotes adherens junction integrity in an autophagy/macroautophagy-dependent manner in ALI/ARDS [9, 16, 22].