SHANK3 and cancer: Many genes have alternative promoters, typically located upstream of the translation start site but also commonly existed within gene bodies.47 Through investigating human and mouse normal brain tissues, one study also suggested that intragenic DNA methylation abolished the activity of alternative promoters of SHANK3 in a tissue- and cell-type-specific manner.48 These results we found further deepen our understanding of the whole landscape of regulatory effects of DNA methylation on ASEs, especially in the context of cancer.