The fact that (a) EGFR, HTT and UBC are among genes composing co‐methylation signatures associated with MSA, and within the same clusters as SNCA or HIP1,12 suggests related molecular functions among those genes, and (b) EGFR, HTT and UBC are experimentally validated protein interactors of SNCA, MOBP and/or HIP1, as seen in our protein–protein interaction network, further supports a functional role for DNA methylation changes in MSA pathogenesis. This evidence concerns the gene HIP1 and multiple system atrophy.