OTUD6B and syndromic intellectual disability: Recent studies found that biallelic pathogenic variants in OTUD6B in 12 individuals from 6 independent families with an intellectual disability syndrome associated with seizures and dysmorphic features.[50, 51] Homozygous OTUD6B knockout mice were dead at the birth day, smaller in size, and had congenital heart defects.[50] Here, we found that OTUD6B knockdown dramatically enhances migration features of human HCC cells in vitro and in vivo.