Notably, while KRAS regulates MYC protein stability through an ERK1/2-dependent mechanism, inhibition of this kinase activates a compensatory pathway through the non-canonical ERK5 to stabilize MYC.156 Long-term inhibition of ERK in KRAS-driven pancreatic cancer was also related to MYC proteasomal degradation, which induced a senescence-like phenotype. Here, MYC is linked to familial pancreatic carcinoma.