AICDA and cancer: A prominent fraction of these mutations arises as a consequence of the off-target activity of enzymes participating in somatic hypermutation (SHM) in immunoglobulin (Ig) genes: DNA/RNA editing cytosine deaminases of the Activation Induced Deaminase (AID)/APOBEC family and the replication/repair of edited sites by DNA polymerases (pols), as deduced by the analysis of the DNA sequence context of mutations in different cancer tissues (Alexandrov et al., 2013; Roberts and Gordenin, 2014; Swanton et al., 2015; Granadillo Rodriguez et al., 2020).