However, transgenic ectopic overexpression mice were effective in exploring the in vivo functions of primate-specific genes, for example, POP2, TMEM14B, ChAT, TOSPEAK, and MCHR1R2, and uncovered novel mechanisms for inflammatory and innate response, neural progenitor proliferation and neurodevelopment, potential cholinergic vulnerability, severe speech impairment, and obesity, respectively (61, 62, 63, 64, 65). The gene discussed is CHAT; the disease is obesity due to melanocortin 4 receptor deficiency.