Moreover, the tumor development kinetic was similar between HT-29 cells (OX1R+/+) and HCT-116 cells (OX1R−/−), indicating that: (i) OX1R expression had no impact on tumor growth in the absence of exogenous orexins; (ii) the presence (or not) of endogenous orexins had no impact on tumor growth; and (iii) the concentration of circulating orexins is too low (about 50 pM) to activate OX1R in tumors [38,39]. Here, HCRT is linked to neoplasm.