AKT1 and neoplasm: Wang et al. (2014) proposed that aberrant SRPK1 expression in either direction induced constitutive Akt activation, thus implying that SRPKs can mediate tumorigenesis independently of their splicing effects, by modulating signaling pathways such as Akt. Yet, while SRPK1 has been reported to intervene in numerous signaling pathways in various cancers (Bullock and Oltean, 2017; Czubaty and Piekiełko-Witkowska, 2017; Nikas et al., 2019) none of these pathways has been implicated in the tumor suppressor function of the kinase nor was correlated with drug responsiveness.