Likewise, a decrease in the amount of functional HNF4α protein, such as that found in heterozygous MODY1 patients [31], activation of signaling pathways [56-61], DNA damage via p53 [62,63], microRNAs [64], diet [35,65,66] and diseases such as colitis and cancer [67,68] could tip the balance between HNF4α protein and potential binding sites, rendering the notion of Alu elements as a sink of HNF4α potentially relevant. This evidence concerns the gene HNF4A and colitis.