Other routes to achieve growth advantage include a) suppression of 5-HT7 action through induction of Gi-coupled receptors, such as 5-HT1E and 1F; b) induction of growth stimulatory 5-HT2C (Gq/11-coupled) [52,53] (observed in MCF7, T47D and in human breast tumors); and c) downregulation of 5-HT synthesis itself, as observed in early stages of primary tumor growth. This evidence concerns the gene HTR2C and breast neoplasm.