The mechanism of how DOCK5 could contribute to obesity is currently unknown, but it has been postulated that DOCK5, a member of the DOCK family of guanine nucleotide exchange factors, could bind to protein phosphatase 2 to inactivate v-akt murine thymoma viral oncogene homolog (Akt) proteins and mitogen-activated protein kinases 1 and 3 (MAPK1 and 3), modulating the anorectic effects of leptin [261]. The gene discussed is MAPK1; the disease is obesity due to melanocortin 4 receptor deficiency.