While it is beyond the scope of this current study, future investigation utilizing our available colon‐specific knockout (KO) mouse models of CHIP and UBXN2A will determine whether the coexistence of UBXN2A and CHIP is necessary and sufficient to slow tumor growth via suppression of mot‐2 and its downstream tumorigenic pathways in a mouse model of CRC. The gene discussed is HSPA9; the disease is colorectal carcinoma.