This suggests that downstream effectors of the KRAS pathway, or related RAS-MAPK signaling components, might be activated through other mechanisms (e.g., upstream receptor tyrosine kinase activity, feedback loops, or crosstalk from other pathways like PI3K/AKT) in a larger subset of melanomas, contributing to the observed prognostic associations and TME modulation. The gene discussed is AKT1; the disease is melanoma.