Since aberrant signaling in KRAS-mutant cancer cells is entirely dependent on the SHOC2-dependent pathway, this suggests that, in contrast to targeting MEK or ERK (which inhibit global ERK signaling), blocking SHOC2 function would interfere only with oncogene-driven ERK activation and would not affect other aspects of normal ERK regulation mediated through SHOC2-independent mechanisms, which would bypass KRAS membrane activation [28]. This evidence concerns the gene KRAS and cancer.