With this approach, we observed a change in flux through the MAPK pathway in response to KH‐4‐43 treatment across in vitro and in vivo ovarian cancer models, which we ascribe to the upregulation of genes within KRAS signalling modules, stabilization of proteins in the MAPK pathway, and increased activity of MAPK‐related kinases like MEK1/2 and BRAF. Here, BRAF is linked to ovarian carcinoma.