Introduction . Recent studies have highlighted the role of non-genetic heterogeneity driving cancer treatment resistance1 , 2 , 3 , 4. Mechanistically, such heterogeneity accumulates continuously via inherent stochasticity in gene expression, and is further strengthened upon each cell division due to uneven partitioning of biomolecules and organelles5. As a result, even isogenic cancer cells exhibit variable drug responses, associated with transient changes in their chr...