In Chronic Neutrophilic Leukemia (CNL) and atypical Chronic Myeloid Leukemia (CML), many CSF3R oncogenic mutations have been reported to segregate to two distinct regions of CSF3R, leading to preferential downstream signaling pathways through the SRC family–TNK2 or JAK kinases [21]. The gene discussed is CSF3R; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.