Consistent with the role of MICAL2 in promoting p53 ubiquitination during colorectal cancer development (Lu et al., 2018), our data indicated that MICAL-L2 knockdown shortened the half-life of c-Myc and decreased c-Myc protein levels, suggesting that MICAL-L2 may promote NSCLC cell proliferation through maintaining c-Myc function. This evidence concerns the gene MICALL2 and non-small cell lung carcinoma.