How does the evidence from previous animal model and functional studies for reduced PARL expression associated with observed and induced T2D (Walder et al., 2005; Tang et al., 2009; Civitarese et al., 2010), square with current results for observed human genomic and expression data implicating ABCC5, but not PARL? We believe the most likely explanation for these observations is that ABCC5 plays a contributory causal role in T2D onset, while PARL dysfunction appears to be a consequence rather than a cause of insulin resistance and disease state. Here, ABCC5 is linked to type 2 diabetes mellitus.