More recently, Ye et al. identified widespread genetic and epigenetic interactions at known T1D susceptibility loci; they showed (in their preprint) that DNA methylation at five loci, i.e., integrin subunit beta 3 binding protein (ITGB3BP), AF4/FMR2 family member 3 (AFF3), protein tyrosine phosphatase non-receptor type 2 (PTPN2), cathepsin H (CTSH), and cytotoxic T lymphocyte-associated protein 4 (CTLA4), is potentially causal to T1D [21]. This evidence concerns the gene AFF1 and type 1 diabetes mellitus.