BUB1B and neoplasm: Additionally, BUB1B-edited clonal cell populations showed a partial to severe loss of BUB1B transcripts, recapitulating the observations from RNAseq analysis of tumor samples from patients carrying BUB1B variants, and also a severe loss of protein abundance, respectively, leading to proliferation-prone premature mitotic exit in a checkpoint-dependent manner, similar to what has been described for MVA variants [19] and supporting the hypomorphic nature of the variant c.1171_1173del.