BTN3A upregulation on cancer cells has been reported to be partially PAM-dependent, where phosphorylation of BTN3A, RHOB, PHLDB2, SYNJ2, and CARMIL1 have been shown to be mainly involved in orchestrating PAM-induced cytoskeletal rearrangements in tumor cells required for spatial and conformational changes in BTN3A [6,26]. This evidence concerns the gene CARMIL1 and cancer.