Given that p53 missense mutations such as p53-R273H are frequent in clinical cases of OSCC, which targets the DNA binding domain of wild-type p53 [56] and compromises the transcriptional activation function [53,54], it is likely that mutations in the upstream transcription activator p53 may lead to decreased levels of ECRG2/SPINK7 protein in clinical cases of human cancers. Here, SPINK7 is linked to cancer.