To further validate whether LCK is a functional downstream target gene of ATMIN in NPC cells, we conducted cell viability assay, clonogenic assay and docetaxel-sensitivity assay, and found that overexpression of LCK could reverse the effects of ATMIN-knockdown-mediated cell proliferation suppression and docetaxel sensitization in NPC cells (Fig. 5E–G). Here, LCK is linked to nasopharyngeal carcinoma.