Since we hypothesized that the compounds binding to the pocket near the α5 helix might prevent the interaction of CaM with KRAS, and since we had previously shown that CaM inhibited KRAS signaling, we first analyzed the effect of P14 on the activation of downstream RAS signaling pathways (RAF/MEK/ERK and PI3K/AKT) in DLD-1 cells (CRC cells carrying one oncogenic KRAS-G13D allele). This evidence concerns the gene KRAS and colorectal carcinoma.