Targeting PDE6D for inhibiting KRAS: A computational approach Rat sarcoma viral oncogene (RAS) has three isoforms namely, Human homologue of RAS, Kirsten rat sarcoma viral oncogene, KRAS and the Neuroblastoma rat sarcoma viral oncogene, NRAS . Of the RAS isoforms, the KRAS gene encodes two protein isoforms, KRAS-4B and KRAS-4A, with each consisting of 188 and 189 amino acids, respectively, due to different clipping of the fourth exon . A wild-type KRAS has a glutamine amino acid at position 61 but, when the amino acid at position 61 is substituted by histidine, it becomes a mutated KRAS. This mutation typically occurs at codons 12 and 13. Significant efforts have concentrated on investigating KRAS mutations especially for the discovery of specific inhibitors that could aid the treatment of KRAS mutation lung cancer . Until recently, KRAS had been widely dubbed "undruggable" due to its lack of deep hydrophobic pockets, making it difficult to bind to small molecules . However, the Food and Drug Administration (FDA) recently approved a small molecule drug, Sotorasib, which specifically targets the RAS G12C mutation . While the advances could help design more broad-spectrum therapeutics, the mutation considered in the development of the drug is only found in low cases of lung cancer (∼13% of lung adenocarcinoma) (AACR). Also, there have been reports of treatment resistance . Hence, there is a need for continuous discovery of drug candidates for treating KRAS mutation lung cancer.