As shown in Figure 3A, consistent with the sustained increase of p-AKT and/or p-ERK (Figure 1B), p-SHP2 levels were obviously elevated in response to low-dose celastrol treatment in all three CRC cell lines, which suggests a critical role of SHP2 in the reactivation of AKT/ERK signaling by celastrol. This evidence concerns the gene AKT1 and colorectal carcinoma.