Once these actively cycling cells later revert to relatively quiescent circulating cells with upregulated BCL2 [72,73], analogously to the transition of germinal center B cells into memory cells [74], any clonal variants with functional BCL2 gene mutations that impair venetoclax binding to BCL2 [14,75] will be venetoclax resistant and could eventually become the dominant CLL subclone [30,70,71]. Here, BCL2 is linked to B-cell chronic lymphocytic leukemia.