Exogenous cannabinoids (like THC and CBD) can enhance or prolong ECS effects, also activating other receptors beyond CB1 and CB2, including transient receptor potential (TRP) channels, such as TRPV1, peroxisome proliferator-activated receptors (PPARs), or other non-cannabinoid targets like GPR55, GPR18, and serotonin receptors, all of which contribute to the broad pharmacological profile of cannabinoids in various therapeutic contexts, including epilepsy, multiple sclerosis, anxiety, and chronic pain (68–71). This evidence concerns the gene GPR55 and multiple sclerosis.