Structural modeling suggested that the recurrent <i>CHEK2</i> p.Leu236Pro variant may introduce steric hindrance affecting protein dimerization.<h4>Conclusions</h4>Our findings and those described in the literature suggest that <i>CHEK2</i> may play a role in the germline origin of childhood pre-B ALL in specific populations. This evidence concerns the gene CHEK2 and acute lymphoblastic leukemia.