Furthermore, unpublished data from our laboratory indicate that protein kinase B (AKT) is subjected to a CSA-dependent ubiquitination that regulates its membrane recruitment and, consequently, its phosphorylation/activation, thus tuning the activation the PI3K-AKT pathway, which is known to be over-activated in many human cancers (Revathidevi and Munirajan, 2019; Uko et al., 2020). This evidence concerns the gene AKT1 and cancer.