In summary, the mechanism of the inhibitory effect of PIK3R1 in PRL is as follows: PIK3R can stabilize PTEN, followed by PTEN, to increase PIP3-to-PIP2 conversion, and attenuate the effect of the PI3K-PIP2-PIP3-AKT pathway [15, 44, 47]; subsequently, IκBa phosphorylation is reduced, IκBa content is increased (IκBa will bind to more NFκB subunits to inactivate NFκB), and the cancer-promoting effect of NFκB is significantly reduced [16, 45, 46]), resulting in reduced expression of MMPs (MMP12/MMP14) to achieve a tumor suppressor effect. Here, NFKB1 is linked to cancer.