RIPK3 and intestinal neoplasm: This is consistent with a recent study showing that when Ripk3−/− mice are crossed with ApcMin/+ mice carrying APC gene mutations (which induce spontaneous development of intestinal tumors), the progeny exhibits increased tumor formation.[9b] Through long‐term follow‐up, we found that various types of spontaneous cancers were developed with high frequency in Ripk3−/− mice (20%) than Ripk3+/+ mice (5.9%), particularly liver, lung, and thymus.