In line with these findings, our data suggest that selective inhibition of ERKT188-phosphorylation may be advantageous in cancer therapy: this strategy efficiently attenuates cancer cell proliferation, may even circumvent compensatory mechanisms to some extent, but most importantly is cardio-safe in vitro and in mice, in contrast to PD98059 or other inhibitors of the Raf/MEK/ERK1/2 signaling cascade such as cetuximab and the clinically used MEK inhibitors trametinib, selumetinib, cobimetinib, and binimetinib. The gene discussed is MAPK3; the disease is cancer.