In fact, because of the decrease in the efficiency of HDR, a switch to other break-repair mechanisms, including non-homologous end joining (NHEJ) and microhomology-mediated break-induced replication (MMBIR) (Hastings et al., 2009; Fitzgerald et al., 2017), could give rise to an increase in the accumulation of chromosomal translocation and CNAs in CD44+/CD24− cancer cells and cells exposed to TGF-β. This evidence concerns the gene CD44 and cancer.