A plausible explanation for how FAM111B overexpression supports cancer progression is that it may influence the apoptotic pathway by upregulating the expression of the anti-apoptotic proteins Bcl-2 and BAG3 or cause indiscriminate degradation of other DNA-associated proteins, including replication or transcription factors (like RFC1 and RPB1), histones and cell-cycle-related proteins such as p16 [4,7,16]. This evidence concerns the gene FAM111B and cancer.