JAK1 and acute lymphoblastic leukemia: Few pieces of evidence are available in the literature regarding the functional consequences of mutations in the protein tyrosine kinase domain of JAK1 in B-ALL, including JAK1S646P that resulted in a high sensitivity to the JAK1/2 inhibitor ruxolitinib in B-ALL patients and JAK1V658F that led to constitutive JAK1 activation in cell lines (Flex et al., 2008; Jeong et al., 2008; Li et al., 2017).