Our data provide insight to the molecular mechanisms of well‐noted immune suppression, dysregulation of myelopoiesis under tumor conditions.22, 30, 31 Previous report showed a role of lamin B receptor in all trans‐retinoic acid induced granulopoiesis, which was accompanied by downregulation of lamin A/C.33 In addition, overexpression of lamin A/C impaired nucleus shape transition which is important for granulopoiesis.34 However, the detailed mechanism of loss of lamin A/C in granulocytic differentiation was largely unknown. Here, LBR is linked to neoplasm.