For example, conditional ATRIP knockout models lacking ATR-interaction domains show markedly reduced monoubiquitination of FANCD2 and FANCI, as well as loss of FANCI phosphorylation—biochemical changes that imply potential disruption of the Fanconi anemia DNA repair pathway by loss of ATRIP function [11,12]. This evidence concerns the gene ATRIP and Fanconi anemia.