Ikaros as a downstream mediator of BCR blockade therapy in B-cell non-Hodgkin lymphoma.

B cell receptor (BCR) complex is essential for B cell development and function, being its downstream effectors involved in the regulation of several biological process such as immune response, cell growth, adhesion, differentiation, survival, cytoskeletal remodeling, and apoptosis [1]. Genetic events leading to BCR constitutive activation and consequent enhancement of tumor cell proliferation and survival, are frequently observed in B-cell non-Hodgkin lymphoma (B-NHL) patients [2]. In the last decade, numerous studies have highlighted that pharmacological targeting of Bruton’s tyrosine kinase (BTK), an apical component of the BCR axis, represents an excellent anti-tumor strategy in chronic lymphocytic leukemia (CLL) and in determined subtype of B-NHL including mantle cell lymphoma (MCL) and follicular lymphoma (FL). Most BTK inhibitors bind irreversibly to the ATP binding site of BTK at the Cys481 amino acid residue, forming a covalent bond that impairs the Editorial