First of all, pharmacological or genetic modulation of several receptors belonging to the eCBome (TRPV1, TRPA1, PPARα, and GPR55) [11–13], administration of eCBome lipid mediators (PEA, OEA) [14–17] and pharmacological blockade of MAGL, FAAH and NAAA [15, 18, 19], enzymes that metabolise eCBome mediators, showed significant anti-inflammatory effects in mouse models of colitis. Here, GPR55 is linked to colitis.