However, it is clear that for a given cancer cell system to take advantage of an increase in intracellular Ca2+ concentration, secondary to CAP agonism over TRPV1, its magnitude should not reach a level that implies mitochondrial dysfunction, a factor that, for its part, it could also be involved in the pleiotropy of the outcome observed with higher concentrations of CAP. This evidence concerns the gene TRPV1 and cancer.