Dear Editor,

Abl1, when fused with BCR, expresses fusion protein BCR‒ABL that underlies the etiology of chronic myeloid leukemia and is therapeutically targeted by Imatinib Mesylate (Khatri et al., 2016). However, the function of proto-oncogene product Abl1 remains not fully understood. This non-receptor tyrosine kinase can be activated by growth factors, DNA damage, oxidative stress, and microbial pathogens (Wang, 2014). Cell-based studies suggest that Abl1 phosphorylates proteins in DNA damage response (DDR) and other signaling pathways, promoting p53 expression as well as cell cycle arrest and apoptosis (Gonfloni et al., 2009). Abl1 deletion leads to runtedness, osteoporosis, and other developmental defects in mice. Interestingly, it has been reported that Abl1 kinase is activated in many solid tumors and Abl1 is implicated in EphB2-mediated intestinal adenoma growth and colorectal cancer (CRC) invasion and metastasis (Kundu et al., 2015; Sonoshita et al., 2015). However, a recent study showed that Abl1 expression is reduced in most CRC patient samples (Uhlen et al., 2015). Thus, the function of Abl1 in CRC initiation warrants further investigation.