Consequently, inhibition of Wee1, the principal gatekeeper of this checkpoint, represents a promising strategy for the treatment of HNSCC, as it may lead to overactivation of CDK1/2, increased replication stress, abrogation of DNA damage checkpoints and cleavage of stalled replication forks by the abnormally activated MUS81 and SLX4 endonuclease complex [228,230]. The gene discussed is WEE1; the disease is head and neck squamous cell carcinoma.