Intriguingly, the murine AAA model also revealed that inihibited functions might be a prime therapeutic target for AAA prevention, according to Huang et al., who discovered that ncRNA PVT1 is involved in AAA progression by sequestering miR-3127-5p and increasing the expression of its target NCKAP1L (Huang et al., 2021). The gene discussed is NCKAP1L; the disease is triple-A syndrome.