For example, the genetic depletion of TRPV1 did not blunt hepatic steatosis but prevented the hepatic injury in chronic alcoholic hepatic disease [257], thus evidencing different roles for TRPV1 in the pathogenesis of different hepatic diseases and making clear that TRPV1 activation is not an obvious pathway to be clinically explored, mainly in the case of MS patients with other comorbidities. The gene discussed is TRPV1; the disease is myeloid sarcoma.