Our results found that ATMIN promotes docetaxel resistance and growth and proliferation through transcriptional activation of LCK in NPC, and overexpression of LCK could reverse the effects of ATMIN-knockdown-mediated cell proliferation suppression and docetaxel sensitization in NPC cells, showing that LCK is a functional downstream target gene of ATMIN in NPC. This evidence concerns the gene LCK and nasopharyngeal carcinoma.