The potential benefit of ASOs for the manipulation of alternative-splicing dependent autophagic functions is limitless, and includes the restoration of ATG5, ATG7, and ATG16L1 wild-type expression in cancer cells, the abrogation of ATG12S or BECN1S expression, the selective expression of PINK1FL to promote mitophagy, and the selective control of ATG14S and ATG14L expression to potentially regulate autophagy induction or completion. The gene discussed is ATG16L1; the disease is cancer.