Mice with ABIN1 UBD domain deletion were embryonic lethality, like ABIN1 knock‐out mice, both of which can be rescued through TNFR1 knock‐out and RIPK1(K45A) mutation.[11] In contrast, Abin1Q478H/Q478H mutant mice are viable but exhibit phenotypes reminiscent of myelodysplastic syndrome (MDS). Here, RIPK1 is linked to myelodysplastic syndrome.