In the present study, we elucidated a role for G0S2 as a tumour suppressor in CML that is downregulated in multiple scenarios of TKI resistance, including TKI non‐responders versus responders (Figure 1A,D), BP‐CML versus CP‐CML (Figure 1A,C), and CP‐CML versus normal myeloid progenitors (Figure 5G). This evidence concerns the gene G0S2 and neoplasm.