Notably, Gpr97—a member of the aGPCR family—was shown to exacerbate AKI in a mouse model by mediating the proinflammatory molecule Sema3A [9,57], and there is evidence of an involvement of Gpr126 in inflammatory processes in other diseases, such as a steady-state stimulation of inflammation in gut-associated lymphoid tissue [58]. This evidence concerns the gene SEMA3A and acute kidney injury.