KRAS and colorectal carcinoma: These findings are in accordance with previous studies conducted by Carvalho and colleagues showing that conditioned media (containing EVs and other soluble mediators) from KRAS-silenced colorectal cancer (HTC116) cells increased ECM components, the migration capacity, and activated CCD-18Co normal-like colon fibroblasts into CAF, suggesting that the inhibition of KRAS might be a potential therapeutic approach for CRC disease [66].