Members of this superfamily appear to regulate a diverse array of cellular events, including the control of GLUT4[8][9] translocation to glucose uptake, cell growth, cytoskeletal reorganization, antimicrobial cytotoxicity,[10] and the activation of protein kinases.

In conditions of obesity and type 2 diabetes, Rac1 signalling in skeletal muscle is dysfunctional, suggesting that Rac1 contributes to the progression of the disease.

[20][21] Activating mutations in Rac1 have been recently discovered in large-scale genomic studies involving melanoma[22][23][24] and non-small cell lung cancer.

[26] Dominant negative or constitutively active germline RAC1 mutations cause diverse phenotypes that have been grouped together as Mental Retardation Type 48.

[28][29][30] For example, Rac1-dependent pathway inhibition resulted in the reversal of tumour cell phenotypes, suggesting Rac1 as a predictive marker and therapeutic target for trastuzumab-resistant breast cancer.