a therapeutic target for many of these diseases. A few recent studies have also exploited targeted therapy to suppress tumor growth by pharmacological inhibition of Rac1 activity in metastatic melanoma and liver cancer as well as in human breast cancer. For example, Rac1-dependent pathway inhibition resulted in the reversal of tumor cell phenotypes, suggesting Rac1 as a predictive marker and therapeutic target for trastuzumab-resistant breast cancer. However, given Rac1's role in glucose transport, drugs that inhibits Rac1 could potentially be harmful to glucose homeostasis. Dominant negative or constitutively active germline RAC1 mutations cause diverse phenotypes that have been grouped together as Mental Retardation Type 48. Most mutations cause microcephaly while some specific changes appear to result in macrocephaly. Interactions RAC1 has been shown to interact with: ARFIP2, ARHGDIA, BAIAP2, FHOD1, FMNL1, IQGAP1, IQGAP2, Myd88, DMPK, NCKAP1, PAK1, PAK3, PARD6A, PARD6B, RICS STAT3, and TIAM1. References Further reading External links RAC1 Info with links in the Cell Migration Gateway