In clinical BC samples, NUMB LOF, due to various molecular mechanisms, is a frequent event, occurring in the majority of BC cases (Figure 1e).[1b,e,r] These mechanisms include aberrant splicing resulting in loss of exon 3‐containing NUMB isoforms and subsequent p53 degradation.[1b] Additionally, hyper‐phosphorylation of NUMB by PKCs (protein kinase C) leads to loss of its asymmetric partitioning at SC mitosis and functional inactivation.[1e] Finally, heightened NUMB ubiquitination leads to its excessive proteasomal degradation as discussed here.[1r]. This evidence concerns the gene TP53 and breast cancer.