Moreover, in the context of neoplasia, tumor cells have evolved various strategies to evade intrinsic apoptosis, such as increasing the expression of antiapoptotic BCL-2 family proteins (BCL-2, BCL-XL, and MCL-1) and harboring extensive genome instability and DNA damage during cell division, leading to the accumulation of self-DNA structures, including micronuclei and chromatin fragments in the cytosol59,60. This evidence concerns the gene BCL2L1 and neoplasm.