Among these, SART3 has been reported to facilitate lung tumorigenesis by modulating the mRNA splicing of CD44 [42]; SF3A1, a core spliceosomal component, has been implicated in the pathogenesis of HCC and colorectal cancer [43]; SF3B1, which is frequently mutated and overexpressed in NSCLC, can confer ferroptosis resistance via the upregulation of SLC7A11 [44]; and SF3B2 has been demonstrated to drive aggressive phenotypes of prostate cancer via the generation of the androgen receptor splice variant AR‐V7 [45]. The gene discussed is CD44; the disease is prostate carcinoma.