Wang et al. showed that pre-S2 deleted proteins could not only upregulate the expression of cyclin A at the transcription level in an ER stress-independent manner, but also induce calcium (Ca2+)-dependent protease μ-calpain-mediated cleavage of cyclin A through the mediation of ER stress, collectively resulting in the elevated production of N-terminus truncated cyclin A (ΔN-cyclin A) in human hepatoma cell lines, in transgenic mouse livers, and in GGHs in HCC patients [43,44]. This evidence concerns the gene CCNA2 and hepatocellular carcinoma.