to blame, experimental technique is partly to blame, and T2*-BOLD contrast is partly to blame. And anyone relying on correlations in resting-state fMRI data as the basis of their hypothesis is on really thin ice. See http://practicalfmri.blogspot.com/2012/1\\... and links therein for more information on just one of the ways that modern scanner hardware exacerbates the problem. What Petrossa said. fMRI is not and never was the appropriate tool to be looking at functional interactions in the autistic brain. This from our 2007 paper: "The tentative but converging fMRI and PET studies discussed above may not provide the necessary temporal resolution to fully characterise the connectivity within and between both local and large scale co-ordinated networks. Contemporary models of connectivity emphasise the role of rapid and transient integration and segregation of both local neuronal clusters or assemblies and large scale co-ordinated networks (Friston, 2000; Engel and Singer, 2001; Varela et al., 2001). "Recent models of cortical 'co-ordination dynamics' (Bressler and Kelso, 2001) claim that the transient re-organisations of coupled local neuronal clusters or assemblies are indexed by changes within a millisecond timescale of patterns in the frequency and phase of oscillatory brain activity, requiring detailed measurement of the spectral characteristics of the cortical signal within very brief time windows (Penny et al., 2002; Makeig et al., 2004). "Contemporary research has focussed on activity in the gamma band (30 -- 60 Hz) which has been measured in tasks demonstrating the binding together of parts to make coherent wholes (see review, Tallon-Baudry and