Given that BIRC5 increases at the centromeres level during G2/M transition and that it is believed to perform its mitotic role through modulation of microtubule function and participation in spindle checkpoint regulation [15] and taking into account that a CDK5RAP1 deficiency suppresses tumor growth through G2/M cell cycle arrest [16], we propose that the treatment with Rapamycin promotes G2/M-phase arrest of oral cancer cells by suppressing BIRC5 and CDK5RAP1. Here, CDK5RAP1 is linked to lip and oral cavity carcinoma.